Toxic exposures to cobalt chloride could occur from dietary, occupational, and medical sources. This study evaluated the ameliorative effect of oral administration of rutin and vitamin E on cobalt chloride (CoCl2)-induced oxidative stress in the brain of rats following exposure to cobalt chloride (CoCl2) toxicity. Wistar rats were randomly divided into five groups. Group 1 received only water, while group 2 received cobalt chloride (300 ppm) in drinking water. Groups 3, 4 and 5 also received cobalt chloride, but were treated with rutin (100 mg/kg body weight), rutin (200 mg/kg BW) and vitamin E (50 mg/kg BW) respectively for seven consecutive days. The rats were euthanized 24 hours after the last treatment. The brain was collected for biochemical and histopathological evaluations. The study demonstrated that cobalt chloride caused a significant (P<0.05) decrease in the activities of superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx) and glutathione level, whereas the levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) increased significantly (P<0.05). However, rutin and vitamin E treatment attenuated CoCl2-induced oxidative stress. Histopathological findings also revealed the ameliorative effect of rutin and Vitamin E on the neuronal damage caused by CoCl2 treatment.

Purpose Anacardium occidentale commonly known as Cashew is a plant that is widely used in African traditional medicine. It is endowed with phytochemical constituents that are responsible for its medicinal properties.Methods Twenty-five male Wistar rats were grouped as follows: Control (Group A), Group B (L-NAME 40 mg/kg), Group C (100 mg/kg Anacardium occidentale extract plus 40 mg/kg L-NAME), Group D (200 mg/kg extract plus 40 mg/kg L-NAME) and Group E (10 mg/kg of Lisinopril plus 40 mg/kg L-NAME). The animals were treated with oral administration of either the extracts or Lisnopril daily for 4 weeks. Neuro-behavioural tests such as the Morris Water Maze and Hanging Wire Grip tests were carried out to evaluate memory/spatial learning and muscular strength, respectively. Makers of oxidative stress, antioxidant enzymes and immunohistochemical staining of Glial Fibrillary Acidic Protein and Ionised Calcium Binding Adaptor molecule 1 were assessed.Results L-NAME administration caused significant increases in biomarkers of oxidative stress, decreased antioxidant status, acetylcholinesterase activity, altered neuro-behavioural changes, astrocytosis, and microgliosis. However, Anacardium occidentale reversed exaggerated oxidative stress biomarkers and improved neuro-behavioural changes.Conclusions Combining all, Anacardium occidentale enhanced brain antioxidant defence status, improved memory and muscular strength, thus, suggesting the neuroprotective properties of Anacardium occidentale.

Objective: The ameliorative effect of Annona muricata in glycerol-induced acute kidney injury in laboratory rats was evaluated. Methods: Thirty albino rats were used and were divided into five of six rats per group. The first (control) group was given distilled water (2 ml/kg) for seven days, while the second (toxicant or glycerol alone) group was given only glycerol (10 ml/kg) on day 8. The third, fourth, and fifth groups received methanol leaf extract of Annona muricata (100 mg/kg), 200 mg/kg dose of the extract, and enalapril (10 mg/kg) respectively for seven days, and on day eight all received glycerol (10 ml/kg). Serum chemistry, histopathology, immunohistochemistry, and changes in blood pressure were indices of toxicity. Results: In the toxicant group, blood pressure increased significantly (p<0.05), but treatment with 200 mg/kg of the leaf extract reversed this. In biochemical analysis, the toxicant group had a significant increase in the levels of oxidative stress markers and decreased levels of some enzymatic and non-enzymatic antioxidants. Treatment with 200 mg/kg of the extract and enalapril reversed the trend. Histopathological changes were seen in the kidney of the toxicant group, but those treated with 200 mg/kg of the extract showed normal kidney histology with no observable lesion. The immunolocalization of angiotensin-converting enzyme and kidney injury molecule-1 in the kidney showed high expression of these proteins in the toxicant group. At the same time, enalapril and the extract caused significant downregulation of their expressions. Conclusion: Results showed that 200 mg/kg dose extract of Annona muricata could confer effective protection on the kidney due to its anti-inflammatory, anti-hypertensive and antioxidant properties.

Hypertension is a chronic cardiovascular disease of extreme and important global concern. It has been established as a leading cause of death especially in humans. The aim of this study was to evaluate the possible antihypertensive effect of a common locally available plant Morinda lucidaagainst L-Nitro-Arginine-Methyl-Ester (L-NAME)-induced hypertension in male Wistar rats. Forty-eight rats were used for the experiment. They were divided into six groups labelled A-F, each containing eight animals. The animals were dosed for six weeks with group A being the control group (normotensive) given feed and water ad libitun; Group B animals were administered L-NAME only, 40 mg/kg (hypertensive); Groups C, D and E were simultaneously treated with L-NAME (40 mg/kg) and Morinda lucida extract in increasing doses of 100 mg/kg, 200 mg/kg and 400 mg/kg, respectively, while Group F were given lisinopril at 20 mg/kg for a period of 6 weeks. From the result, there was significant increase in systolic, diastolic, and mean arterial blood pressure in the hypertensive group compared to the normotensive group and hypertensive treated groups. Hypertension caused significant (p<0.05) increases in oxidative stress markers, including malondialdehyde (MDA), protein carbonyl (PC), hydrogen peroxide (H O ), while reducing the activities of superoxide dismutase (SOD), and serum nitric oxide (NO) levels. Also, serum myeloperoxidase (MPO), blood urea nitrogen and creatinine were increased with high expression of cardiac injury biomarkers such as cardiac troponin and angiotensin 2 type 1 receptor. These indicated oxidative stress, cardiac damage because of hypertension, most especially in the untreated hypertensive group. The co-treatment of hypertensive rats with Morinda lucida extract caused reduction in markers of oxidative stress and inflammation and normalized blood pressure parameters. The findings from this study suggest the possibility of using Morinda lucida extract as a novel antihypertensive agent.

Acute kidney injury (AKI) is a life-threatening abrupt disruption in kidney function. The pathophysiological mechanisms of AKI are poorly understood. Also, there are currently no effective drugs to treat AKI. Phytochemicals from Moringa oleifera plants exhibit antihypertensive, cholesterol-lowering, diuretic, and hepatoprotective properties. This study aims to determine if Moringa oleifera extract can ameliorate rhabdomyolysis-induced AKI and its possible mechanisms of action. Experimental rats were randomly divided into five groups. Rhabdomyolysis was induced by intramuscular glycerol injection. Group A received distilled water only. Group B received distilled water, followed by 50% glycerol on the 8th day. Group C and D received 50 and 100 mg/kg methanol stem extract of Moringa oleifera (orally) for seven days and glycerol on the 8th day. Group E received 100 mg/kg of methanol stem extract of Moringa oleifera alone for seven days and normal saline on the 8th day. Necropsy was performed 24 h after glycerol treatment. Blood and kidneys samples were collected for biochemical, histopathological, and immunohistochemical analyses. Significant decreases in superoxide dismutase, glutathione peroxidase, glutathione S-transferase, glutathione, protein thiols, and non-protein thiols were observed in animals treated with only glycerol when compared with the control groups. Glycerol treatment also caused a significant increase in markers of AKI and inflammation, including creatinine, nitric oxide, urea, hydrogen peroxide, malondialdehyde, protein carbonyl, and advanced oxidative protein products. Immunohistochemical staining of renal NF-ƙβ and KIM-1 was also elevated in glycerol-treated rats. Treatment with methanol stem bark extract of Moringa oleifera ameliorated glycerol-induced oxidative stress, kidney damage, and inflammation. The methanol stem extract of Moringa oleifera alleviated rhabdomyolysis-induced AKI in rats through its antioxidant and anti-inflammatory properties.

Hypertension is a condition with chronic elevation of blood pressure and a common preventable risk factor for cardiovascular disease with attendant global morbidity and mortality. The present study investigated the novel antihypertensive and neuroprotective effect of Naringenin on L-NG-Nitro arginine methyl ester (L-NAME) induced hypertension together with possible molecular mechanism of action. Rats were divided into four groups. Rats in Group A were normotensive. The hypertensive group (Group B) received 40 mg/kg) of L-NAME alone while Groups C and D were concurrently administered Naringenin (50 mg/kg) or Lisinopril (10 mg/Kg) together with L-NAME orally for 3 weeks. Blood pressure parameters, markers of oxidative stress and renal damage were measured. The immunohistochemistry of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme were also determined. Results indicated significant increases in malondialdehyde, advanced oxidation protein products, protein carbonyl contents and decrease in serum nitric oxide bioavailability in hypertensive rats. Furthermore, there were significant increases in serum myeloperoxidase, urinary creatinine, albumin and blood urea nitrogen in hypertensive rats in comparison to hypertensive rats treated with either Naringenin or Lisinopril. Immunohistochemistry reveal significant expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme in hypertensive rats. However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Collectively, Naringenin offered a novel antihypertensive and neuroprotective effect through down regulation of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme.

Introduction: Cisplatin (CP)-induced toxicity involves oxidative stress and Picralima nitida is rich in natural antioxidants hence its methanol leaf extract was used to mitigate the toxic effect of CP.Methods: Forty rats divided into four groups of 10 rats per group were used as follows: group A (normal saline), group B (CP 10 mg/kg), group C [Methanol Leaf Extract of Picralima nitida (MLEPN), 100 mg/kg and CP 10 mg/kg], and group D (MLEPN 200 mg/kg and CP 10 mg/kg). All administrations were done by oral gavage with the volumes of the treatments administered determined by the average weight of the rats in each group except CP, which was given intraperitoneally. Administration of normal saline and MLEPN lasted for seven consecutive days after which a single dose of CP was given on day 8. All animals were sacrificed 72 hours after CP administration. On day 9, blood pressure measurement was taken, and changes in body weight were determined. On day 10, blood samples were taken for serum chemistry, and kidneys, liver, and heart were harvested from the animals for Serum assay, histopathology, and immunohistochemistry, respectively.Results: The extract improved weight changes caused by CP and reversed the toxic changes produced by CP on serum chemistry, oxidative stress, and histopathology. The extract caused a significant decrease in the levels of nuclear factor kappa beta, cardiac troponin, and mineralocorticoid receptors (MCRs). However, it increased the protein expression of Nrf2 compared to the toxicant group.Conclusion: The extract exhibited anti-inflammatory, antioxidant, and anti-renin properties.

Environmental and occupational exposure to chromium compounds has become a potential aetiologic agent for kidney disease through excessive generation of free radicals, induction of apoptosis and exaggerated inflammatory responses. These are some pathophysiologic mechanisms of potassium dichromate (K Cr O ) toxicity with attendant nephrotoxicity and cardiotoxicity. The cardioprotective and nephroprotective effects of Luteolin, a known potent antioxidant were evaluated in this study as described; Group A (normal saline), Groups B (30 mg/kg K Cr O ), Group C (Luteolin 100 mg/kg and K Cr O 30 mg/kg), and Group D (Luteolin 200 mg/kg and K Cr O 30 mg/kg), respectively. Markers of antioxidant defense system, oxidative stress, blood pressure and micronucleated polychromatic erythrocytes (MnPEs) were determined. Immunohistochemistry of Kidney Injury molecule (Kim-1), nuclear factor erythroid 2-related factor 2 (Nrf2), and cardiac troponin I (CTnI) were also determined. Our results showed that administration of K Cr O increased systolic, diastolic and mean arterial blood pressures, markers of oxidative stress, the frequency of micronucleated polychromatic erythrocytes together with a significant reduction in serum nitric oxide bioavailability. Immunohistochemical staining revealed higher expression of renal Kim-1 and cardiac troponin I in rats intoxicated with K Cr O . However, lower expression of renal and cardiac Nrf2 were also observed in Luteolin co-administered rats. Furthermore, co-treatment with Luteolin restored blood pressure parameters, with concomitant reduction in oxidative stress indicators, augmented in vivo antioxidant status and improved serum NO levels. Lowered expressions of Kim-1, CTnI and up-regulation of both cardiac and renal Nrf2, and reduced frequency of micronucleated polychromatic. Taken together, this study demonstrates for the first time the antihypertensive, cardioprotective, nephroprotective and antigenotoxic effects of Luteolin against potassium dichromate induced-toxicity through antioxidant and radical scavenging mechanisms.

Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating fluoride-induced hypertension and nephrotoxicity with clofibrate, a peroxisome proliferator–activated receptor-alpha (PPARα) agonist. For this study, forty male Wistar rats were used and randomly grouped into ten rats per group, control, sodium fluoride (NaF; 300 ppm) only, NaF plus clofibrate (250 mg/kg) and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. The administration of NaF was by drinking water ad libitum, while clofibrate and lisinopril were administered by oral gavage. Administration of NaF induced hypertension, and was accompanied with exaggerated oxidative stress; depletion of antioxidant defence system; reduced nitric oxide production; increased systolic, diastolic and mean arterial pressure; activation of angiotensin-converting enzyme activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); and testicular apoptosis. Treatment of rats with clofibrate reduced oxidative stress, improved antioxidant status, lowered high blood pressure through the inhibition of angiotensin-converting enzyme activity, mineralocorticoid receptor over-activation, and abrogated testicular apoptosis. Taken together, clofibrate could offer exceptional therapeutic benefit in mitigating toxicity associated with sodium fluoride.

A sudden decrease in the functionality of the kidney with concomitant structural damage and functional loss is known as acute kidney injury (AKI), with some of the potential causes having to do with a focal mismatch between oxygen and nutrient delivery to the nephrons. Increased energy demands on account of cellular stress is another cause [Kellum et al 2021]. AKI occurs when renal function is acutely decreased, so waste products accumulate within the body, making the body unable to maintain electrolyte, acid-base, and water balance [Bhatraju et al 2020]. As a result of the decrease in the kidney's ability to carry out its perfusion activity, the epithelial cells lost the ability to maintain sufficient intracellular ATP for essential processes. This ATP depletion leads to cell injury. Depending on the severity of ATP depletion, cell death by necrosis or apoptosis could occur [Biswas et al 2018]. Studies have actually demonstrated that the pathogenesis of glycerol-induced AKI involves myoglobin toxicity, reactive oxygen species, inflammation, and redox-active iron [Al Asmari et al 2017; Wu et al 2017]. Currently, animal models of glycerol-induced AKI are widely used [Mousleh et al 2018]. Glycerol injection into the muscle causes the release of myoglobin and other muscle contents into the circulation, ultimately resulting in AKI. Twenty animals divided into four groups of five animals per group were used. Group I served as control while group II received glycerol on day 8 only. Groups III and IV were administered with pioglitazone and ramipril for 7 days respectively and on day 8 received glycerol. On day 9 blood samples were collected for serum biochemical analysis of markers of oxidative stress, enzymatic and non-enzymatic antioxidants, creatinine and blood urea nitrogen. Animals were sacrificed thereafter; and kidney tissues were harvested for histopathology and immunohistochemistry. Expression of caspase 3, renin receptor, NF-κB, and KIM-1 were carried out. Results from this study showed that ramipril and pioglitazone significantly inhibited markers of oxidative stress while also significantly increased the levels of enzymatic and non-enzymatic anti-oxidant markers. These drugs caused decreased levels of creatinine and BUN. While massive leucocytes infiltration and congestion of the kidney occurred in the toxicant group, it was mild in the ramipril treated group and the two drugs significantly inhibited the expressions of the four proteins, which were highly expressed in the toxicant group. Thus ramipril and pioglitazone have nephroprotective effect and mitigated acute kidney injury through their anti-inflammatory, anti-apoptosis, anti-renin and anti-oxidant properties. Some References Al Asmari AK, Al Sadoon KT, Obaid AA, Yesunayagam D, Tariq M. Protective effect of quinacrine against glycerol-induced acute kidney injury in rats. BMC Nephrol. 2017; 18:41. Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Hans- Joachim A. Acute kidney injury. Disease Primers 2021; 7: 52.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). This virus has become a global pandemic with unprecedented mortality and morbidity along with attendant financial and economic crises. Furthermore, COVID-19 can easily be transmitted regardless of religion, race, sex, or status. Globally, high hospitalization rates of COVID-19 patients have been reported, and billions of dollars have been spent to contain the pandemic. Angiotensin-converting enzyme (ACE) 2 is a receptor of SARS-CoV-2, which has a significant role in the entry of the virus into the host cell. ACE2 is highly expressed in the type II alveolar cells of the lungs, upper esophagus, stratified epithelial cells, and other tissues in the body. The diminished expressions of ACE2 have been associated with hypertension, arteriosclerosis, heart failure, chronic kidney disease, and immune system dysregulation. Overall, the potential drug candidates that could serve as ACE2 activators or enhance the expression of ACE2 in a disease state, such as COVID-19, hold considerable promise in mitigating the COVID-19 pandemic. This study reviews the therapeutic potential and pharmacological benefits of the novel ACE2 in the management of COVID-19 using search engines, such as Google, Scopus, PubMed, and PubMed Central.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent for the Coronavirus Disease 2019 (COVID-19). The COVID-19 pandemic has created unimaginable and unprecedented global health crisis. Since the outbreak of COVID-19, millions of dollars have been spent, hospitalization overstretched with increasing morbidity and mortality. All these have resulted in unprecedented global economic catastrophe. Several drugs and vaccines are currently being evaluated, tested, and administered in the frantic efforts to stem the dire consequences of COVID-19 with varying degrees of successes. Zinc possesses potential health benefits against COVID-19 pandemic by improving immune response, minimizing infection and inflammation, preventing lung injury, inhibiting viral replication through the interference of the viral genome transcription, protein translation, attachment, and host infectivity. However, this review focuses on the various mechanisms of action of zinc and its supplementation as adjuvant for vaccines an effective therapeutic regimen in the management of the ravaging COVID-19 pandemic. Practical applications The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent for the Coronavirus Disease 2019 (COVID-19), has brought unprecedented untold hardship to both developing and developed countries. The global race for vaccine development against COVID-19 continues with success in sight with attendant increasing hospitalization, morbidity, and mortality. Available drugs with anti-inflammatory actions have become alternative to stem the tide of COVID-19 with attendant global financial crises. However, Zinc is known to modulate several physiological functions including intracellular signaling, enzyme function, gustation, and olfaction, as well as reproductive, skeletal, neuronal, and cardiovascular systems. Hence, achieving a significant therapeutic approach against COVID-19 could imply the use of zinc as a supplement together with available drugs and vaccines waiting for emergency authorization to win the battle of COVID-19. Together, it becomes innovative and creative to supplement zinc with currently available drugs and vaccines.

The anti-proliferative effect of the methanol leaf extract of Picralima nitida on Human Colorectal Adenocarcinoma Cell lines (HT-29) was investigated using the Cell Titer 96 MTT assay because Picralima nitida is a therapeutic herb used in ethnomedicine for the management of several disease conditions. Cells were cultured to confluence, trypsinized, and plated in 96-well plates for cell proliferation assay. Twenty four hours after plating, cells were treated with various concentrations (62.5, 125, 250 μm) of the extract along with the control in the presence or absence of Calphostin C (10 μm) or Tyrphostin (10 μm) and cultured for 24–72 h to determine effects of treatment on cell growth. MTT assay was performed at 24, 48 and 72. MTT assay was performed over 3 days. In vitro antiproliferative study showed that the extract at all concentrations caused cytotoxicity of the HT29 cells. The extract in the absence of the enzyme inhibitors caused a higher cell inhibition than in their presence with the 62.5 μm/ml causing a higher inhibitory effect on the cells. The ability of the methanol leaf extract of Picralima nitida with a higher antiproliferative property in the absence of the enzyme inhibitors is a pointer to its cytotoxic efficacy. It was thus concluded from this study that the plant extract from Picralima nitida has anti-proliferative/cytotoxic effect hence further evaluation on the constituents responsible for this effect may be explored.

Environmental and occupational exposure to chromium compounds has become potential aetiologic agent for kidney disease with excessive generation of free radicals, apoptosis, and inflammatory. These pathophysiologic mechanisms of potassium dichromate (K2 Cr2 O7 ) have been well correlated with nephrotoxicity and cardiotoxicity. The cardioprotective and nephroprotective effects of Luteolin, a known potent antioxidant were evaluated in this study with 40 healthy rats in four experimental groups: Group A (normal saline), Groups B (30 mg/kg K2 Cr2 O7 ), Group C (Luteolin 100 mg/kg and K2 Cr2 O7 30 mg/kg), and Group D (Luteolin 200 mg/kg and K2 Cr2 O7 30 mg/kg), respectively. Markers of antioxidant defense system, oxidative stress, blood pressure and micronucleated polychromatic erythrocytes (MnPEs), immunohistochemistry of Kidney, injury molecule (Kim-1), nuclear factor erythroid 2-related factor 2 (Nrf2), and cardiac troponin I were determined. Administration of K2 Cr2 O7 increased blood pressure parameters in systolic, diastolic and mean arterial blood pressures, markers of oxidative stress, and frequency of micronucleated polychromatic erythrocytes, together with reduction in serum nitric oxide level. Renal Kim-1 and cardiac troponin I expressions were higher, but lower expressions of renal and cardiac Nrf2 were recorded with immunohistochemical analysis. Pre-treatment with Luteolin restored blood pressure parameters, with concomitant reduction in oxidative stress indicators, augmented antioxidant mechanisms and serum Nitric oxide level, lowered the expressions of Kim-1, cardiac troponin I and up-regulated of both cardiac and renal Nrf2, reduced the frequency of micronucleated polychromatic erythrocytes. Taken together, this study therefore demonstrates the cardioprotective, nephro protective and antigenotoxic effects of Luteolin through antioxidantive and radical scavenging mechanisms.

Acute renal failure (ARF) has been documented as a life-threatening disease with high morbidity and mortality. We investigated the protective effect of Luteolin against ARF. In this study, forty-male Wistar albino rats were randomly divided into four groups (n = 10). Group A received normal saline. Group B received glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Groups C and D were pretreated with Luteolin 100 and 200 mg/kg for 7 days, and thereafter administered Glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Administration of glycerol significantly increased systolic blood pressure, diastolic blood pressure and mean arterial pressure. Renal protein carbonyl and xanthine oxidase increased significantly while significant reduction in the activity of renal glutathione peroxidase, glutathione S-transferase and glutathione reductase was observed in the glycerol intoxicated rats. Furthermore, administration of glycerol led to significant increases in serum creatinine and blood urea nitrogen together with reduction in nitric oxide (NO) bioavailability. Immunohistochemistry revealed that glycerol intoxication enhanced expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin (CTnI). However, Luteolin pretreatment normalized blood pressure, reduced markers of oxidative stress, renal damage, and improved NO bioavailability. Luteolin also downregulated the expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin. Together, Luteolin might open a novel therapeutic window for the treatment of acute renal failure and cardiac complication.

Background and Aim: High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats. Materials and Methods: The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), Group D was fed with cocoa-feed compounded with 8% salt for 4 weeks after uninephrectomy, and Group E was uninephrectomized rats on a normal diet. The left kidneys of animals in Groups C, D, and E were removed by surgery. After 4 weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues. Results: Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress. Conclusion: These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.

The anti-diabetic property of aqueous leaf extract of Moringa oleifera was performed in streptozocin-induced diabetic rats using serum chemistry, histology and immunochemical parameters as indices of diabetes. The blood glucose level of the diabetic untreated group continues to increase while that of the treated group after 21 days decreased. While the animals in the diabetic untreated group experienced increase in the levels of markers of organ damage when compared to the control group (P values < 0.0001). ALT increased from 61.83±1.5 to 96.1±22.4, AST was 225.1±26.6 from 172.6±13.9, ALP 13.5±0.006 to 13.6±0.002, UREA 1.0±0.08 to 3.0±0.4, their reduction was observed in the extract-treated groups. ALT reduced from 96.1±22.4 to 73.70±9.7; AST from 225.1±26.6 to 184.4±18.2; ALP from 13.6±0.002 to 13.6±0.01; UREA from 3.0±0.4 to 2.0±0.4. Treatment with the extract significantly reduced markers of oxidative stress in the kidney [hydrogen peroxide (898.8±6.26 to 688.0±13.7), malondialdehyde (640±0.1 to 600±0.2) and protein carbonyl (548.4±1.5 to 458.1±1.6)]; heart [hydrogen peroxide (389.4±1.8 to 358.2±1.5), malondialdehyde (264.0±0.5 to 122.0±0.3), protein carbonyl (196.8±0.5 to 162.7±3.5)]; and liver [hydrogen peroxide (119.36±3.2 to 103.94±10.7), malondialdehyde (236.0±0.4 to 73.0±0.2), protein carbonyl (269.3±1.0 to 174.2±1.1) respectively. The levels of antioxidants were reduced in the diabetic untreated group but there was increase in the Moringa treated group. Glucose transporter 4 (GLUT 4) was down regulated in the diabetic untreated group while it was well expressed in the treated groups. The histology of pancreas and liver showed varied levels of infiltration of inflammatory cells, congestion and necrotic lesions, but these were mild in the treated groups. The result shows that the extract does have an anti-diabetic effect with the decrease in the levels of blood glucose and markers of oxidative stress as well as increase in the amount of antioxidants in the treated group when compared to the diabetic untreated group. More importantly, the extract caused upregulation of GLUT 4, which is relevant in reversing insulin resistance in the same manner as pioglitazone, the standard antidiabetic agent used in this study.

Moringa oleifera popularly referred to as wonder plant is a medicinal plant with a remarkable variety of therapeutic purposes. The aim of this study was to assess the ameliorative effect of Moringa oleifera on glycerol-induced acute kidney injury in rats thus renewing interest in the development of new treatment plans. Glycerol (50% v/v in sterile saline, intramuscular) was used to induce acute kidney injury. Group A (control group) received distilled water only, the group B animals (toxicant group) received glycerol alone on the 8th day, and groups C and D animals were given 50 mg/kg and 100 mg/kg of methanol stem extract of Moringa oleifera respectively for seven days and glycerol on the 8th day. Group E animals on the other hand received 100 mg/kg of methanol stem extract of Moringa oleifera alone for seven days and on day 8 received normal saline. To assess renal damage and possible ameliorative effects of the extract, serum blood urea nitrogen (BUN), creatinine, myeloperoxidase, advanced oxidative products, malondialdehyde, superoxide dismutase, reduced glutathione, and protein carbonyl were determined. Histopathological analysis of kidney tissues and immunohistochemical analysis of KIM-1 and NF-ҝB expressions were also carried out on kidney tissues. The results showed that methanol stem bark extract of Moringa oleifera improves glycerol-induced acute kidney injury by inhibiting markers of inflammation, oxidative stress and renal damage by modulating KIM-1 and NF-ҝB signaling pathways. In conclusion, the methanol stem extract of Moringa oleifera blunts glycerol-induced acute kidney injury in rats through its anti-oxidant and anti-inflammatory properties.

This study assessed the therapeutic effects of chloroquine on diabetes and its renal, cardiac and hepatic complications. A single intraperitoneal streptozotocin (STZ) injection in an animal model was used for this study. Blood glucose level, body weight, markers of oxidative stress such as malondialdehyde (MDA), hydrogen peroxide (H2O2) generation, protein carbonyl, nitric oxide (NO), reduced glutathione and antioxidant enzymes such as superoxide dismutase, glutathione peroxidase were evaluated. Histopathology of various organs was done to evaluate structural changes. Immunohistochemical changes using CTnI, Kim-1, PPARγ and Nrf2 were also performed. It was shown that chloroquine administration significantly improved blood glucose levels and body weight. Structural changes such as necrosis, inflammatory cell infiltration, and congestion induced by STZ injection were ameliorated with chloroquine treatment. Untreated diabetic animals showed marked increase in levels of oxidative stress and inflammatory markers such as MDA, H2O2, NO, MPO, and depletion in both non-enzymatic and enzymatic antioxidant defense system, upregulation of Kim1, CTnI, downregulation of PPARγ and Nrf2. Treatment with chloroquine ameliorated renal and cardiac injury coupled with increased expressions of Kim-1 and CTnI. It can therefore be postulated that chloroquine exhibited antidiabetic property through upregulation of PPARγ. Its anti-inflammatory and antioxidant properties were confirmed through the upregulation of Nrf2 and improved antioxidant status.