Introduction Diabetes mellitus is a chronic metabolic condition characterized by hyperglycemia due to either insulin resistance, lack of insulin production, and/or secretion. The global rates of infection are increasing, especially in low- and middle-income countries; thus, exploring novel and safer therapeutic options has become essential. This review aims to compile and analyze existing data on the anti-diabetic properties of selected medicinal plants, focusing on their phytochemical composition, molecular mechanisms of action, and potential therapeutic roles in glucose homeostasis. Methods A comprehensive literature search was conducted using databases such as Scopus, ScienceDirect, and Google Scholar. Sixteen medicinal plants traditionally used for diabetes management were identified and examined based on multiple experimental studies. Results Phytochemicals such as flavonoids, polyphenols, saponins, and terpenoids from these plants exhibit anti-diabetic effects through multiple mechanisms: modulation of glucose transporters ( e.g. , GLUT4), activation of insulin signaling pathways ( e.g. , PI3K/Akt), inhibition of digestive enzymes ( e.g. , α-amylase, α-glucosidase), promotion of insulin secretion, and mitigation of oxidative stress. Discussion Notably, compounds like quercetin, kaempferol, berberine, and gymnemic acid have shown significant promise. Conclusion Medicinal plants present a rich source of bioactive compounds with multi-targeted mechanisms relevant to diabetes management. Further pharmacological investigations are necessary to establish their therapeutic efficacy and safety, enabling the development of phytochemical-based interventions for diabetes.
Alzheimer's disease (AD)is a complex and multifactorial neurodegenerative disorder characterized by common pathogenic features, such as the development of amyloid-β (Aβ) plaques and the formation of neurofibrillary tangles from hyperphosphorylated tau proteins. Although the cholinergic hypothesis, which focuses on the cognitive role of acetylcholine, remains a fundamental concept, recent studies have reported that neuroinflammation and oxidative stress play pivotal roles in the pathology of AD. Besides these pathways, aging, diverse diseases, environmental factors, and genetic conditions are well-known risk factors for AD. Currently, no disease-modifying treatment exists for AD. The available therapies provide only symptomatic relief and are often associated with adverse side effects. Meanwhile, growing evidence suggests that dietary interventions rich in anti-inflammatory and antioxidant compounds can modulate inflammatory cytokines and neutralize free radicals, thereby offering a promising approach to mitigate AD risk and potentially delay its onset. Future research should focus on developing novel therapeutic strategies that specifically target the restoration of the oxidative–inflammatory balance, moving beyond symptomatic relief to address the key pathological pathways in AD.
Introduction Plasma cell neoplasms are characterized by the production of paraproteins. These paraproteins can interfere with routine biochemical assays performed using conventional wet chemistry platforms, leading to erroneous results, misinterpretation, and delays in diagnostic evaluation. Objective The objective of this study is to investigate the extent of interference caused by monoclonal proteins (M-proteins) in calcium, magnesium, and phosphate assays, and to quantify the degree and significance of such interference. Methods This is an observational case–control study. Test samples containing M-proteins and control samples without M-proteins were analyzed using both wet chemistry and dry chemistry methods in parallel. Data were evaluated using paired t-tests in the test group and unpaired t-tests in the control group. Passing–Bablok regression and Bland–Altman difference plots were employed to assess method comparison and agreement. Results Control samples without paraproteins demonstrated no significant method-related differences in calcium and magnesium assays, whereas a minor method difference was observed for phosphate. In contrast, test samples containing paraproteins exhibited statistically significant interference in calcium, magnesium, and phosphate assays when analyzed using conventional wet chemistry methods. Discussion Paraproteins can significantly interfere with biochemical assays (p < 0.05) performed using traditional wet chemistry analyzers. In comparison, dry chemistry platforms demonstrate greater resilience to such interference, thereby offering a more reliable alternative for minimizing paraprotein-induced assay variability in patients with plasma cell neoplasms. Conclusion These findings suggest that dry chemistry may serve as a suitable alternative to conventional wet chemistry for minimizing paraprotein-related assay interference.
Background Azo dyes are widely used in the textile industry for fabric coloring; however, their potential to induce oxidative stress poses significant health concerns. Nrf2 (Nuclear factor erythroid 2-related factor 2) is a pivotal oxidative stress marker. Methods This study involved 90 male workers: 45 exposed to azo dyes and 45 unexposed (control group). The exposed group was subdivided based on exposure duration into three categories: EG1 (1–10 years), EG2 (11–20 years), and EG3 (>20 years). Nrf2 activity was measured using ELISA, while Total Antioxidant Capacity (TAC) and Total Oxidative Status (TOS) were assessed via spectrophotometry. Results Exposed workers exhibited significantly higher Nrf2 activity (mean ± SD: 2.06 ± 0.68) than the control group (1.58 ± 0.41, P = 0.000). Additionally, the exposed group showed lower TAC (1.39 ± 0.1 vs. 1.50 ± 0.06, P = 0.000) and higher TOS (0.14 ± 0.05 vs. 0.11 ± 0.03, P = 0.002). Nrf2 levels increased with the duration of exposure (EG1: 1.68 ± 0.37, EG2: 1.92 ± 0.44, EG3: 2.60 ± 0.81), while TOS levels rose (EG1: 0.10 ± 0.04, EG2: 0.13 ± 0.03, EG3: 0.19 ± 0.02), and TAC levels decreased (EG1: 1.49 ± 0.06, EG2: 1.38 ± 0.05, EG3: 1.30 ± 0.09). Discussion The elevation of Nrf2, along with increased TOS and reduced TAC levels, suggests a compensatory antioxidant response to ongoing oxidative burden. These changes reflect the biological impact of chronic exposure to azo dyes. Conclusion These findings highlight the role of azo dyes in inducing oxidative stress among textile workers, emphasizing the urgent need for protective measures to mitigate occupational health risks.
Hepatitis C is a global issue, causing acute and chronic hepatitis with high mortality. Drug abusers are at the highest risk. This study compares liver enzyme levels in HCV patients using smoked opium derivatives versus oral methadone to assess prognosis and treatment response. Materials and Methods: This descriptive-analytic, retrospective study included 100 participants from a sample of 350, selected based on inclusion criteria. Data were collected via a researcher-designed checklist and analyzed using STATA14 with descriptive and inferential statistics. Covariance analysis was used to control for confounders like time and age. The mean levels of liver enzymes (ALT and AST) in patients with chronic HCV who consumed methadone orally were 77.25 (SD=8.26) and 78.325 (SD=7.91), respectively. The mean levels of ALT and AST in patients with chronic HCV who smoked heroin were 50.71 (SD=4.88) and 53 (SD=4.69), respectively. The effect of two confounding variables, age, and duration of drug use, on the level of liver enzymes was controlled using covariance analysis. The level of significance of the model was 0.007, which was less than 0.05, indicating that the level of AST and ALT in patients with chronic HCV who consumed methadone orally and smoked heroin was different. HCV patients using oral methadone show higher ALT and AST levels and greater liver damage than heroin smokers. Alternative treatments to methadone are recommended to reduce liver damage and improve outcomes in these patients.
Background Capsaicin is a natural alkaloid and one of the main active components found in spicy peppers, responsible for their hot taste. It possesses antioxidant and anti-tumor properties. In this study, the effect of capsaicin on the expression of genes involved in apoptosis, such as Bax, Bcl2, Caspase3, p53, PPARγ, Nrf2, and the activity of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, was investigated in LS-180 and HCT-116 human colorectal cancer cell lines. Methods Human colorectal cancer cell lines (LS-180 and HCT-116) were treated with various concentrations of capsaicin for 24 hours. The expression levels of genes, including Bax, Bcl2, Caspase3, Nrf2, PPARγ, and p53, were determined using the Real-time PCR method, and the activity of antioxidant enzymes was measured using colorimetric assays. Results Analysis of gene expression results showed that capsaicin increased the expression levels of Bax, Bcl2, Caspase3, and p53 in both cell lines, but this increase was statistically significant in the LS-180 cell line. Capsaicin also significantly increased the expression of Nrf2 and PPARγ in both cell lines. The activity of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, was increased in both cell lines compared to the control. Conclusion It appears that capsaicin may play a role in inducing apoptosis and reducing the proliferation of colorectal cancer cells through the upregulation of Nrf2, PPARγ, and p53 gene expression and the increase in antioxidant enzyme activity. Additionally, the upregulation of Bax and Caspase 3 expression suggests a potential mechanism for capsaicin-induced apoptosis and the reduction of colorectal cancer cell growth.
Advancements in modern medicine have not fully resolved the complexities associated with wound healing, particularly for chronic wounds, such as diabetic ulcers and burn injuries. Effective wound management necessitates not only the regeneration of damaged tissue but also minimizing scar formation. In this context, natural compounds derived from plants have emerged as promising candidates for enhancing wound healing. Ethnobotanical research has demonstrated that various herbal extracts possess properties that could significantly improve wound healing outcomes. This review explores the potential of these natural compounds, focusing on their mechanisms of action, efficacy in clinical and preclinical studies, and the challenges that still need to be addressed. By synthesizing findings from traditional medicinal practices and contemporary scientific research, this review aims to provide a comprehensive understanding of how natural compounds can contribute to more effective wound healing strategies. In this review, widely used and studied plants are discussed, along with their ability to induce wound healing through all the phase and their mechanism of action.
Background Cancer stem cells (CSCs) represent a relatively small subset of cells within tumors, capable of self-renewal and associated with metastasis and cancer recurrence. While conventional chemotherapy targets actively dividing bulk tumor cells, dormant CSCs remain unaffected and survive. Hypoxia or deprivation of oxygen supply is a common feature of solid tumors, which plays a critical role in metastatic progression and CSC maintenance. However, the cellular responses to hypoxia might be influenced by many factors, including the severity, duration, and other specific characteristics of this stress. Objective In our study, we assessed the impact of long-term hypoxia on the CSCs population in 5 cell lines representing 5 different tumor types. Methods We assessed and characterized the effect of oxygen concentration on CSC population using the sphere formation assay. The protein levels in tumor spheres were examined by western blot analysis. Results Long-term hypoxia inhibited sphere formation by PC-3 and MDA-MB-231 CSCs. Moreover, chronic hypoxic stress suppressed cell proliferation in tumor spheres in all 5 tested cell lines: SNB-19, HCT116, MDA-MB-231, NCI-H460 and PC-3. This effect was accompanied by PCNA downregulation in tumorspheres derived from NCI-H460 and PC-3 cells. Conclusion The prolonged hypoxic conditions impede tumor sphere formation by PC-3 prostate CSCs, primarily through the downregulation of PCNA levels. The specific cellular response to hypoxia depends on the duration and, supposedly, other specific features of this stress.
Background Colorectal cancer stands as the prevailing form of cancer affecting the digestive tract. Antioxidants have been observed to influence the activity of antioxidant enzymes and elevate the expression of genes within the apoptosis pathway. Consequently, this dynamic interplay appears to suppress the progression of colorectal cancer. Objectives This study aimed to evaluate the effect of astaxanthin on the expression of effective genes in apoptosis and the activity of antioxidant enzymes in colorectal cancer HCT-116 cells. Methods In this experimental investigation, HCT-116 cells underwent treatment with varying concentrations of astaxanthin for a duration of 24 hours. Subsequently, the expression levels of BAX, Bcl2, and caspase 3 genes were quantified using real-time PCR, while malondialdehyde levels and antioxidant enzyme activity were analyzed utilizing calorimetric methods. Results The analysis of gene expression outcomes revealed that astaxanthin elicited significant effects. It augmented the expression of BAX and caspase-3 genes, thereby promoting apoptosis while concurrently downregulating the expression of the Bcl2 gene. Consequently, this led to a decrease in malondialdehyde concentration, serving as an oxidative stress index. Additionally, the antioxidant activity of superoxide dismutase, catalase, and glutathione peroxidase showed significant increases in these treated cells. Conclusion Astaxanthin appears to modulate the antioxidant defense system within cancer cells. This is achieved by enhancing the activity of antioxidant enzymes while concurrently inhibiting cell growth and proliferation. Furthermore, the compound triggers apoptosis in HCT-116 cell lines, further contributing to its potential as a therapeutic agent in cancer treatment.
Background Deep Vein Thrombosis (DVT) is a high-risk condition that necessitates the use of oral anticoagulants for treatment. Warfarin, a common anticoagulant, exhibits varying levels of efficacy and toxicity among individuals. The CYP2C9 gene promoter polymorphism significantly influences the dosage requirements, a factor that remains underexplored in the contemporary Indian population. Objectives This study aimed to investigate the influence of CYP2C9 gene polymorphisms on warfarin dosage due to pharmacogenetic effects. Specifically, it examined the prevalence of the CYP2C9 polymorphic alleles *2 and *3 and their correlation with warfarin dosage in the South Indian Population (NCAP). Methods The study involved 96 warfarin-treated patients to determine the genotype frequency of common CYP2C9 polymorphisms. The genotypes of CYP2C92 and CYP2C93 polymorphisms were analyzed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. A one-way analysis of variance (ANOVA) was conducted to ascertain dosage variation across genotypes. Results The study found that the frequencies of the two variations were 25.5% for CYP2C92 and 40.6% for CYP2C93. Patients with a homozygous wild-type genotype for CYP2C9 (*1/*1) required a daily warfarin dose of 4.07 ± 1.75 mg, significantly higher than the *1/*2, *1/*3 (2.93 ± 2.03 mg, p <0.0001) and *2/*2, *2/*3, and *3/*3 patients (1.54± 1.05 mg, p = 0.002). The study also revealed a distinct allelic frequency of CYP2C9 polymorphisms in the study population compared to other populations. Conclusion Given the relatively high prevalence of CYP2C9 polymorphisms in the studied population, practitioners should consider these findings to minimize the risk of bleeding when prescribing warfarin.
Background Sports training causes physiological changes in almost every body system; the more successfully these changes accomplish the functional adaptation required to execute the physical load effectively while conserving energy, the greater performance improvement may be anticipated. For training programs to be effective and boost performance in any sport, they must consider the nature and kind of the sport as well as a study of the performance conditions. Methods This research investigated how a 5-week, specially designed high-intensity interval training (HIIT) programme affected the aerobic ability of adolescent female basketball players. It also investigated how physical characteristics, skill qualities, heart impulse, oxygen distribution rates, and energy expenditure indices relate to one another. Lastly, research was conducted on the significance of urea-ketone energy consumption. Results A basketball-specific high-intensity training program lasting twelve sessions most likely reduced the time for the 20-meter speed test (Pre: 3.22 ± 1.72, Post: 3.02 ± 1.75 Sec) and improved the standing long jump test (Pre: 1.55 ± 0.49, Post: 1.65 ± 0.35 cm) and vertical jump test (Pre: 27.83 ± 6.40, Post: 31.42 ± 7.23 cm). Conclusion Oxygen uptake (VO2), VO2/Kg, carbon dioxide generation (VCO2), respiratory exchange ratio (RER), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) were all positively impacted by the training sessions. After 12 sessions, young female basketball players' aerobic performance is improved with HIIT tailored specifically for basketball.
Background Methotrexate (MTX) is a commonly used chemotherapy drug with known nephrotoxic effects, including the potential for acute kidney injury. However, the precise mechanism through which MTX induces nephrotoxicity remains unclear, though oxidative stress and direct toxic effects on renal tubules are believed to play key roles. Recent studies suggest that calcium channel blockers may offer promise in slowing down the progression of chronic kidney diseases. Objective The purpose of this study was to explore the potential of Amlodipine, a calcium channel blocker, to alleviate acute kidney injury caused by the administration of MTX in rats. Methods Three groups of twenty-four male Wistar rats were randomly assigned: Group 1—the control group was given normal saline orally. Group II, underwent five days of continuous administration of a single intraperitoneal (IP) dosage of 20 mg/kg MTX. The same dosage of MTX was given to Group III followed by an oral dose of Amlodipine at 5 mg/kg over the same period. Upon completion of the experiment, serum biochemical parameters, renal damage markers, oxidative stress, inflammatory markers, and kidney tissue histology were assessed. Results The results indicate that MTX administration significantly increased the levels of serum biochemical parameters, renal damage markers, inflammatory markers, oxidative stress markers, and induced alterations in kidney histology. However, the administration of Amlodipine following MTX treatment protected against these changes. Conclusion Amlodipine exhibits therapeutic potential in mitigating MTX-induced kidney injury in rats and its associated side effects.
Background: SARS-CoV-2 is a virus responsible for the COVID-19 pandemic that began in late 2019. This pandemic has had a devastating impact worldwide, resulting in over 6.95 million deaths. The development of effective vaccines against the virus is crucial for preventing infection and reducing the severity of the disease. Objective: This study aimed to obtain the recombinant receptor-binding domain (RBD) and the nucleocapsid (N) proteins of SARS-CoV-2 as well as assess the immunogenicity of the combination of these recombinant proteins. Methods: The recombinant plasmids encoding the receptor-binding domain (RBD) of the spike protein of the Omicron variant and the nucleocapsid protein of SARS-CoV-2 were cloned into the yeast Pichia pastoris . The optimal fermentation conditions were established for recombinant P. pastoris strains. The methods for the isolation and purification of the target recombinant RBD and nucleocapsid proteins were developed. The immunogenicity of the purified recombinant proteins was evaluated by injecting them into mice and analyzing the specific IgG antibody responses using ELISA. Results: The study found that RBD and N proteins, as well as their combination, showed antigenic specificity and were highly immunogenic in mice. The immunogenicity was measured by determining the antibody titer, which represents the concentration of antibodies produced in response to the antigen. The antibody titers were 1:60000 for both RBD and N proteins, and 1:80000 for their combination. Conclusion: These findings suggest that the expressed proteins could be potential candidates for the development of vaccines or immunological diagnostic test kits for combatting or detecting the Omicron variant of SARS-CoV-2.
Objective: The COVID-19 epidemic resulted in a global crisis of public health. Therefore, the possibility of prevention, leading to reduced infection and/or an improved disease state, is the subject of intensive attention. The novelty of this study is the direct evaluation of vitamin D levels with the risk of COVID-19 infection. Background: Currently, several nutraceuticals, including vitamin D, beta-glucan, and some minerals, are being studied for their role in stimulating immunity. Our study focused on the relationship between levels of vitamin D in immunodeficient patients and the risk of the development of COVID-19. Method: In this study, patients were supplemented with vitamin D. Results: In a group of 71 patients, we found that patients with vitamin D levels below 30 ng/ml had an increased risk of COVID-19 development and more severe disease progress. In patients with blood levels over 40 ng/ml, we consistently found high levels of protection against COVID-19 infection. Conclusion: The most important finding is that vitamin D levels above 40 ng/ml result in the reduction of risks of serious clinical manifestation of COVID-19 infection.
Antimicrobial peptides (AMPs) are small proteins that protect against bacterial and fungal infections. Various organisms, including plants, animals, and bacteria, produce them. The HMGB-1 (HMGB-1) protein is produced by both immune cells and bacteria, and its main role is to facilitate the recognition of foreign agents, such as bacteria, by the immune system. AMP can protect against infections by interacting with HMGB-1. This enhances their protective capabilities and reduces inflammation associated with bacterial infections.
Background: Type 2 diabetes is caused by unhealthy lifestyles, such as consuming foods rich in simple sugars and lack of exercise. One of the treatment therapies for this disease is α-glucosidase inhibitors. Some strains of the lactic acid bacteria (LAB) group typically exhibit α-glucosidase inhibitory activity, antimicrobial activity, acids and bile salt tolerance, and probiotic status. Objective: This study aims to isolate LAB from naniura, characterize and test its activity as an α-glucosidase inhibitor, as well as identify those with the highest activity. Methods: The method used to molecularly identify potentially good LAB was through the amplification of the 16S rRNA gene. Results: This study obtained a total of 9 strains using BAMA codes 1, 2, 3, 4, 5, 6, 7, 8, and 9. The cocci cell activity, gram-positive, and antibacterial activity of BAMA 4 against E.coli was 7.54 mm, while against S. aureus was 8.05 mm. The percentage of viability in acid and bile salt is 28.7% and 68.6%, respectively. Additionally, the proportion of α-glucosidase inhibition is 65%. Discussion: The BAMA 4 strain is a species of Pediococcus acidilactici . Pediococcus is a genus of gram-positive lactic acid bacteria in the Lactobacillacea family. Conclusion: BAMA 4 strain produced antibacterial optimally and its cells survived the growth in acid and bile conditions. The percentage of probiotics was relevantly high in this activity. This study will be helpful for other in-vivo research.
Background: Fusion of the last two enzymes in the pyrimidine biosynthetic pathway in the inverse order by having COOH-terminal orotate phosphoribosyltransferase (OPRT) and NH 2 -terminal orotidine 5′-monophosphate decarboxylase (OMPDC), as OPRT-OMPDC, has been described in many organisms. Objective: The study aimed to select the optimum host cell and temperature for expressing the recombinant fusion OMPDC-OPRT having the enzymatic activity. Methods: We constructed gene fusions of the human malaria parasite Plasmodium falciparum OMPDC-OPRT (1,836 bp) in the pTrcHisA vector and expressed it as a 6xHis-tag bifunctional protein in three Escherichia coli strains (BL21(DE3), TOP10, Rosetta) at 18°C and 25°C. The recombinant bifunctional protein was partially purified by Ni-nitrilotriacetic acid affinity chromatography and confirmed via Western blot and LC-MS/MS. The enzyme kinetics of OPRT and OMPDC was assessed. Results: Specific enzymatic activities of both OPRT and OMPDC domains expressed in E. coli BL21(DE3) cells were approximately eight-to-nine-fold higher than those in the TOP10 cells at 18°C. However, the specific activities of both domains expressed in the TOP10 cells were twice higher than those of the BL21(DE3) cells at 25°C. Very low and no enzymatic activities were observed when the constructed vector was expressed in the Rosetta cells at both induction temperatures. The bifunctional enzyme had specific activities of the OPRT and OMPDC domains in a ratio of 1:2. Kinetic study values of the OPRT domain in the bifunctional OMPDC-OPRT enzyme were found to be relatively low at µM level and at the perfect catalytic efficiency ( k cat /K m ). Conclusion: The recombinant fusion of OMPDC-OPRT exhibited a high expression level of E. coli BL21(DE3) at 18°C. The kinetic parameter is greater than 10 8 M -1 s -1 .
Background: Mitochondrial dysfunction in retinal pigment epithelium (RPE) is a pathogenic factor in age-related macular degeneration (AMD). Improvement of mitochondrial function may ameliorate RPE bioenergetics status, which may in turn nourish the retinal photoreceptors against degenerative loss. Objective: The purpose of this study is to examine the G-protein coupled receptor (GPCR) antagonistic drug CM-20 in modulating mitochondrial function in RPE cells. Methods: Human-derived ARPE-19 cell line was differentiated to improve RPE morphology. Dose response of CM-20 was performed to examine mitochondrial membrane potential (MMP). Secondary validation with multiplexed live-cell mitochondrial imaging was performed. Protection of CM-20 to mitochondria against oxidative stress was detected under co-treatment with hydrogen peroxide. Results: Treatment with CM-20 elicited a dose-dependent increase of MMP. Multiplexed live-cell mitochondrial imaging showed consistent increase of MMP at an optimal concentration of CM-20 (12.5 μM). MMP was significantly reduced under hydrogen peroxide-induced oxidative stress and treatment with CM-20 showed rescue effects to MMP. Conclusion: CM-20 increases mitochondrial function and protects mitochondria under oxidative stress. As both GPCRs and mitochondria are potential drug targets, retinal neuroprotective testing of CM-20 is warranted in animal models of retinal degeneration.
Hypoxia-inducible factors (HIFs) are transcription factors that initiate the expression of cellular processes to cope with hypoxic conditions. HIFs are principal regulators of hypoxic adaptation, regulating gene expression involved in glycolysis, erythropoiesis, angiogenesis, proliferation, and stem cell function under low O2. HIFs may play a pivotal role in tumor survival and metastasis in cancer formation and growth. Likewise, HIFs play a key role in microbial pathogenesis, particularly in host-pathogen interaction. Because of the role that HIF-1alpha plays in the biology of cancer and infections, it is a potential therapeutic target not only for malignant growth but also for parasitic infection. Several reports have demonstrated the up-regulation of host cellular HIFs due to infection-induced hypoxia. Hypoxia-inducible pathways have attracted great interest in the down-regulation of prolyl hydroxylase for treating inflammatory diseases and infections by viruses, protozoa, or bacteria, among other pathogens. Interestingly, increasing evidence suggests that HIFs play an important regulatory role in inflammation. For example, in macrophages, HIFs regulate glycolytic energy generation and optimize innate immunity, control pro-inflammatory gene expression, mediate the killing of pathogens and influence cell migration. Therefore, a good understanding of the biochemical mechanism of hypoxia signaling pathways will shed more light on how it could help identify and develop new treatment strategies for cancer and parasitic diseases, including viral, bacterial, fungal and protozoa infections.
