This study investigated the protective effects of zingerone (ZIN) against thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats (n = 10 per group). HE was induced by TAA (200 mg/kg, intraperitoneally (i.p.)) on days 1 and 3, and rats were treated with ZIN (25 or 50 mg/kg/day, intragastric gavage (i.g.)) for 14 days. Serum biochemistry, oxidative stress, inflammatory markers, ER stress-related proteins, apoptosis indicators, histopathology, and behavioral outcomes were evaluated TAA administration markedly increased whole-blood ammonia concentrations together with serum activities of the hepatic injury biomarkers ALT, AST, ALP, GGT, and LDH compared with the Control group, while ZIN treatment significantly improved these parameters. ZIN reduced malondialdehyde (MDA) levels and restored antioxidant defenses (SOD and GSH) in both liver and brain tissues. Pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) were elevated after TAA exposure, whereas IL-10 was reduced; ZIN dose-dependently reversed these changes. In addition, TAA increased ER stress markers (GRP78, CHOP, ATF6, XBP1, IRE1, and PERK) and apoptosis-related Bax and caspase-3 expression, which were significantly suppressed by ZIN. In brain tissue, ZIN preserved BDNF expression and reduced GFAP immunoreactivity. Behavioral impairments, including anxiety-like behavior and locomotor deficits, were significantly improved at 50 mg/kg. Overall, ZIN exhibited dose-dependent hepatoprotective and neuroprotective effects in TAA-induced hepatic encephalopathy, as evidenced by attenuation of oxidative stress, inflammation, ER stress, and apoptosis. This study provides an integrated evaluation of ZIN in hepatic encephalopathy, extending prior findings in other hepatotoxicity models, including CCl₄ and cadmium-induced injury, as well as related phytochemical studies in HE.

Vancomycin (VCM)-induced nephrotoxicity remains a clinically important adverse effect associated with oxidative injury, inflammatory signaling, mitochondrial dysfunction, and tubular cell death. This study investigated whether Morin (MOR) could modulate these toxicological mechanisms in a rat model of VCM-induced renal injury. Fifty adult male Sprague Dawley rats were randomly divided into five groups and treated for 7 consecutive days. On day 8, kidney tissues were collected for biochemical, histopathological, immunohistochemical, immunofluorescence, Western blot, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) analyses. VCM administration induced marked renal injury, as evidenced by increased malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, decreased superoxide dismutase (SOD) and glutathione (GSH) levels, severe tubular degeneration, necrotic changes, and structural disruption in renal tissue. In addition, VCM significantly increased tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), receptor for advanced glycation end products (RAGE), and NLR family pyrin domain-containing 3 (NLRP3) levels, while reducing interleukin-10 (IL-10) expression. Apoptotic injury was confirmed by increased Bcl-2-associated X protein (Bax) and caspase−3 levels together with decreased B cell lymphoma 2 (Bcl-2) expression. Moreover, Kelch-like ECH-associated protein 1 (Keap-1) was upregulated, whereas nuclear factor erythroid 2-related factor 2 (Nrf-2), heme oxygenase 1 (HO-1), sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), phosphoinositide 3-kinase (PI3K), mechanistic target of rapamycin (mTOR), and AKT serine/threonine kinase 2 (AKT2) levels were downregulated, accompanied by increased forkhead box protein O1A (FOXO1A) expression. MOR treatment, particularly at 100 mg/kg, significantly ameliorated these alterations by reducing oxidative injury, restoring endogenous defense systems, attenuating inflammatory responses, suppressing apoptosis, and markedly improving histopathological lesions. MOR also attenuated VCM-associated alterations in Keap-1/Nrf-2/HO-1-, SIRT1/PGC1α-, and PI3K/AKT2/mTOR/FOXO1A-related markers. Collectively, the nephroprotective effects of MOR were associated with coordinated changes in oxidative, inflammatory, apoptotic, and cell-survival markers in this experimental model.

Lead is a highly toxic heavy metal and an environmental pollutant. Lead exposure causes damage and dysfunctions in organs. In tissues exposed to lead, ROS increase, resulting in oxidative stress, inflammation and apoptosis. In this study, we aimed to investigate the protective effects of Borago officinalis (BO) against lead, whose toxic effects are well-established. In this study, 40 Sprague-Dawley rats were used. The rats were randomly divided into 5 groups. The groups were determined as control, BO100, Pb (20 mg/kg), Pb+BO50 and Pb+BO100. After the experimental procedures were completed, the tissues were transported in cold chain and stored in -80 deep freezer until the experiments were performed. Keap-1 level was determined in spleen tissue using Western blot method. At the same time, IL-1β, IL-10, NF-ĸB, Bax, Bcl-2, Caspase-3 levels were determined by RT-PCR method. BO administration stimulated Keap-1 level in relation to oxidative stress. While BO suppressed IL-1β and NF-ĸB levels, it stimulated IL-10 level, which are anti-inflammatory markers. BO also suppressed Bax and Kaspas-3 levels, while significantly stimulating Bcl-2 level. With these effects, it was observed that BO had anti-oxidant, anti-inflammatory, anti-apoptotic effects in the spleen tissue of rats treated with lead acetate.

This study examined the antioxidant, anti-inflammatory, and neuroprotective effects of melatonin (MEL) against acrylamide (ACR)-induced neurotoxicity in Sprague-Dawley rats. The experimental groups included control, ACR, MEL10+ACR, MEL20+ACR, and MEL20. MEL at doses of 10 and 20 mg/kg, and ACR at 50 mg/kg, were administered intraperitoneally for 14 days. On the 15th day, locomotor activity was assessed, and brain tissues were analyzed biochemically, molecularly, and histopathologically. ACR exposure decreased locomotor activity, increased malondialdehyde (MDA) and reduced glutathione (GSH) levels, indicating oxidative stress, and decreased antioxidant enzyme activities (SOD, GPx, CAT). High-dose MEL (MEL20+ACR) effectively reduced lipid peroxidation and restored antioxidant enzyme activities. MEL treatment also suppressed proinflammatory cytokines (TNF-α, IL-1β, IL-6) and neuronal nitric oxide synthase (nNOS), demonstrating anti-inflammatory effects. Furthermore, MEL mitigated ACR-induced neurotoxicity by reducing acetylcholinesterase (AChE) and monoamine oxidase (MAO) levels. ER stress markers (GRP78, ATF4, ATF6, sXBP1, CHOP) and apoptotic markers (Bax, Caspase-3) were elevated following ACR exposure but were suppressed by MEL. Additionally, MEL reduced ACR-induced increases in 8-hydroxy-2-deoxyguanosine (8-OHdG) and glial fibrillary acidic protein (GFAP), markers of DNA damage and astrocyte activation, respectively. These findings underscore the potential of MEL to counteract ACR-induced neurotoxicity through its comprehensive antioxidant, anti-inflammatory, and neuroprotective actions.

Objective: To investigate the protective effects of naringin on doxorubicin (DOX)-induced liver injury. Methods: A total of 50 male rats were allocated into five groups: the control group, the DOX group, the DOX groups treated with 50 mg/kg and 100 mg/kg of naringin by gastric lavage for 10 days, as well as the group treated with 100 mg/kg of naringin alone. Liver and serum samples were collected for biochemical, histopathological, and molecular analyses, including liver enzyme activity, oxidative stress markers, inflammation, apoptosis-related proteins, and DNA damage indicators. Results: Naringin attenuated DOX-induced elevation in liver enzyme activity and inflammation markers while enhancing antioxidant activities. Naringin also activated the Nrf2-HO-1 signaling pathway, with the most pronounced effect in the high-dose naringin group. In addition, naringin modulated apoptotic signaling by downregulating the expression of PI3K-AKT and BAX, and upregulating Bcl-2, as well as reduced the level of 8-OHdG. Histopathological evaluation showed that DOX-induced structural liver alterations, such as cellular degeneration and necrosis, were notably attenuated by naringin treatment. Conclusions: Naringin treatment exerts protective effects against DOX-induced liver injury through its antioxidative, anti-inflammatory, and anti-apoptotic effects.

The aim of this study was to investigate p-Coumaric acid (PCA) as a protector in detecting oxidative and targeted damage in the elongation tissue of rats induced by bisphenol A (BPA). BPA is an environmental pollutant widely used in many areas. The widespread use of this substance increases its transmission to humans. BPA causes damage to many tissues and organs. One of the most frequently damaged organs is the kidney. In this study, fifty healthy male rats were used to determine the effects of BPA and PCA. A total of five experimental groups were formed with ten animals in each group. Group 1 was set as the Control, Group 2 as BPA, Group 3 as BPA+PCA50, Group 4 as BPA+PCA100, and Group 5 as PCA100. The experiment lasted 14 days. Hematoxylin eosin staining and ELISA analyses were performed on kidney tissues at the end of the experiment. Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and nitric oxide (NO) levels were determined in the kidney tissues by ELISA analysis. It was observed that kidney MDA and NO levels increased in the groups administered BPA while SOD and GSH levels decreased. Histopathologically, degeneration and necrosis in the tubular epithelium, glomerular atrophy, and hyperemia in the vessels were observed in the kidney tissues of the BPA groups. In the BPA+PCA groups it was seen that PCA prevented the negative effects of BPA in a dose-dependent manner, and helped in the maintenance of values close to the control group.

Objective: To explore the possible effects of naringin on acrylamide-induced nephrotoxicity in rats. Methods: Sprague-Dawley rats weighing 200-250 g were randomly divided into five groups. The control group was given intragastric (i.g.) saline (1 mL) for 10 d. The acrylamide group was given i.g. acrylamide in saline (38.27 mg/kg titrated to 1 mL) for 10 d. The treatment groups were administered with naringin in saline (50 and 100 mg/kg, respectively) for 10 d and given i.g. acrylamide (38.27 mg/kg) 1 h after naringin injection. The naringin group was given i.g. naringin (100 mg/kg) alone for 10 d. On day 11, intracardiac blood samples were obtained from the rats when they were under anesthesia, after which they were euthanized. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbent assay was used to quantify malondialdehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase, tumor necrosis factor-β, nuclear factor-κB, interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2, kidney injury molecule-1, mitogen-activated protein kinase-1, and caspase-3 in kidney tissues. Renal tissues were also evaluated by histopathological and immunohistochemical examinations for 8-OHdG and Bcl-2. Results: Naringin attenuated acrylamide-induced nephrotoxicity by significantly decreasing serum urea and creatinine levels. Naringin increased superoxide dismutase, glutathione, glutathione peroxidase, and catalase activities and decreased malondialdehyde levels in kidney tissues. In addition, naringin reduced the levels of inflammatory and apoptotic parameters in kidney tissues. The histopathological assay showed that acrylamide caused histopathological changes and DNA damage, which were ameliorated by naringin. Conclusions: Naringin attenuated inflammation, apoptosis, oxidative stress, and oxidative DNA damage in acrylamide-induced nephrotoxicity in rats.

5‐fluorouracil (5-FU), a pyrimidine analogue anticarcinogenic agent, is widely used in the solid tumors treatment. Use of the 5-FU causes cardiotoxicity. Our aim in this study investigations effects of Quercetin and Rutin on ECG parameters in the 5-FU-induced cardiotoxicity in rats. In the present study used male rats. Rats were divided randomly to eight group. The control group was given intragastric corn oil for 14 days. The 5-FU group rats were given ig corn oil for 14 days and injected intraperitoneal the single dose of 5-FU(50 mg/kg) on the eleventh day. The Q50+5-FU and Q100+5-FU groups were given ig 50 mg/kg and 100 mg/kg Q for 14 days, respectively and these groups were injected single dose of 5-FU(50 mg/kg) on the 11th days of Q application. The group Q100 was Q(100 mg/kg-ig) for 14 days. The Rutin50+5-FU and Rutin100+5-FU groups were injected ig 50 mg/kg and 100 mg/kg of the Rutin for 14 days, respectively. These groups were injected single dose of 5-FU(50 mg/kg) in the 11th days of Rutin application. The Rutin 100 group was given Rutin(100 mg/kg-ig) for 14 days. In the end of experimental application recorded to ECGs of the rats. 5-FU administration rats were observed that it was caused sinus tachycardia and ST elevation. Also, in the 5-FU group QRS segment was shorter and the duration and amplitude of the P was different from other groups. In both doses of Q and Rutin were prevented these changes and our findings were seen the consistent with the literature.

: This study aimed to investigate the protective effects of Naringin in Cyclophosphamide (CYP)-induced cardiotoxicity in rats. In the study, forty male adult Sprague Dawley rats weighing approximately 200-250 g were used. Rats were divided into 5 experimental groups as control, CYP, Naringin50+CYP, Naringin100+CYP and Naringin100. Control and CYP groups were administered to intragastric (i.g.) saline for 10 days. Also, the CYP group was given a single dose of CYP (200 mg/kg, intraperitoneal (i.p.)) on the 10th day. Naringin50+CYP and Naringin100+CYP groups were administered i.g. 50 and 100 mg/kg doses of Naringin for 10 days, respectively, and was given a single dose of CYP (200mg/kg, intraperitoneal (i.p.)) on the 10th day. Naringin100 group was administered to Naringin (100mg/kg), i.g.) for 10 days. ECG was recorded under anesthesia, and intracardiac blood samples were taken. Troponin I, creatine kinase (CK) and creatine kinase-MB (CK-MB) parameters were examined in serum samples. As a result of the necropsy, preparations were prepared by routine cardiac tissue follow-up method for histopathological examination. For the detection of DNA damage in the cardiac tissue, 8-OHdG expression was investigated. CYP has been shown to have cardiotoxic effects on ECG values, cardiac enzymes, and cardiac histopathology of rats. In this study, it was determined that Naringin has a protective effect in CYP-induced cardiotoxicity in rats.

Bu çalışmada siklofosfamid (CYP) ile uygulanan ratlarda kan ve serum örneklerinde Naringin (NA)’in antioksidanlar ve serbest radikaller üzerine protektif etkilerinin araştırılması amaçlandı. Araştırmamızda yaklaşık 200-250 g ağırlığında, 40 adet erkek erişkin Sprague Dawley rat kullanıldı ve her bir grupta 8 ratın bulunduğu 5 grup oluşturuldu. Kontrol grubuna 10 gün boyunca intra gastrik (i.g.) serum fizyolojik (1 ml) verildi. CYP grubuna 10 gün boyunca i.g. serum fizyolojik verildi ve 10. gün tek doz intra peritonal (i.p.) CYP (200 mg/kg) enjekte edildi. NA50+CYP ve NA100+CYP gruplarına 10 gün boyunca sırasıyla serum fizyolojikte çözdürülmüş 50 ve 100 mg/kg dozunda i.g. NA uygulandı ve NA’nın son enjeksiyondan sonra tek doz CYP (200 mg/kg, i.p.) enjekte edildi. NA100 grubuna ise 10 gün boyunca 100 mg/kg dozunda i.g. NA uygulandı. Deneyin 12. gününde ratlar tiopental sodyum (20 mg/kg) ile anestezi altına alınarak intra kardiyak kan örnekleri alındı ve dekapite edildiler. Ratlardan elde edilen kan ve serum örneklerinde Total Antioksidan Durumu (TAS), Total Oksidan Durumu (TOS), Oksidatif stres indeksi (OSİ) ve 8-Hydroxydeoxyguanosine (8-OHdG) parametreleri analiz edildi. CYP’nin ratlarda oksidatif stresi artırdığı, antioksidanları baskıladığı ve DNA hasarına yol açtığı tespit edildi. NA’nın farklı dozlarının, CYP’nin sebep olduğu oksidatif stresi baskıladığı, antioksidan miktarını artırdığı ve DNA hasarını önlediği belirlendi.

Anaplazmozis koyunlarda sıklıkla görülen, kan hücrelerini enfekte eden artropod kaynaklı ve ekonomik kayıplara neden olabilen paraziter bir hastalıktır. Bu çalışma Anaplazmozis ile enfekte koyunlarda bazı serum inflamasyon markır seviyelerini değerlendirmek için planlanmıştır. Yapılan araştırma için kullanılacak olan kan örnekleri, Van Büyükşehir Belediyesi Mezbahanesi’ne getirilen 20 sağlıklı ve 20 Anaplazmozis’li koyundan sağlandı. Kontrol ve hasta gruplarının belirlenmesi, hastalığın klinik belirtileri, giemsa boyalı kan frotileri ve serolojik yöntem (cELISA) yardımıyla yapıldı. Toplanan 91 koyunların ait serum örneği Anaplazma spp. türlerinin antikorlarının varlığı yönünde serolojik olarak incelendiğinde %73.6’sı (67/91) Anaplazmozis yönünden seropozitif bulundu. Kan frotisinde Anaplazma etkenleri görünen ve ELISA inhibisyon değeri yüksek çıkan koyunların kanları analizler için kullanıldı. Anaplazmozis’li koyunlar teşhis edildikten sonra pozitif ve negatif olarak gruplandırıldı. Pozitifliği tespit edilen 20 koyun serumunda granülosit makrofaj koloni uyarıcı faktör (GM-CSF), interlöykin-1β (IL-1β), interlöykin-6 (IL-6), tumor nekroz faktör- alfa (TNF-α) düzeyleri elisa kiti ile kit prosedürüne göre belirlendi. Proinflamasyon parametrelerinden serum IL-1β (ng/L), TNF-α (ng/L), GM-CSF (ng/L) düzeylerinin negatif gruba göre istatiksel olarak yükseldiği tespit edildi. Anaplazmaya karşı gelişen inflamasyon ile ilgili mekanizmaların incelenmesi, ileride geliştirilecek immunoterapi araştırmaları için Anaplazma enfeksiyonlarının teşhis ve önlemeye yönelik çalışmalara katkı sağlayacağı düşünülmektedir.

Objective: To investigate the effects of probiotic bacteria on cisplatin (CP)-induced nephrotoxicity. Methods: In the present study, 50 Sprague-Dawley rats were used and randomly divided into five groups including control, CP, probiotic bacteria treatment groups with different doses (0.5 and 1 mL) and only probiotic bacteria group. After CP and probiotic administration on seven days, rats sacrificed under anesthesia on the eighth day. The serum urea, creatinine, and blood urea nitrogen levels were analyzed. In renal tissue, malondialdehyde levels, superoxide dismutase and glutathione activity, interleukin-8, interleukin-1β and tumor necrosis factor-alpha levels were determined and histopathological and immunohistochemical changes were also examined. Results: According to results, urea, creatinine and blood urea nitrogen levels as well as kidney weights increased in CP group. Also, CP induced inflammation, oxidative stress, DNA damage and apoptosis in kidney tissue and caused histopathological changes. Administration of the high dose of probiotic bacteria could prevent these changes and damages. Conclusions: This study reveals that probiotic bacteria has protective effects on CP-induced renal damage in rats.

Cisplatin, an anticarcinogenic agent, is reported to have side-effects that include hepatotoxicity. Probiotics are live microorganisms which, when administered in adequate amounts, confer a health benefit on the host. Thus, the objective of this study was to investigate the protective effects of probiotic bacteria against cisplatin-induced hepatotoxicity. Sprague-Dawley male rats weighing 220-250g were used in the study. Fifty rodents were assigned to five groups (10 in each group). The groups received treatments for seven days. On day eight, the rats were decapitated, and blood and liver tissue were taken. When the liver tissue was assessed for oxidative stress, that in Group II was found to have significantly increased stress compared to that in the other groups (p<0.050). It was determined that serum AST, ALT, and LDH levels; the SOD activity; and the GHS levels in liver homogenates from CP-treated rats were significantly decreased when compared with the other groups (p<0.05). The MDA levels in liver homogenates from CP-treated rats were significantly increased when compared with other groups (p<0.05). Cytokine levels (IL-8, IL-1 beta, and TNF-alpha) in the liver tissue were significantly elevated in the Group II compared to those in Group I (p<0.050). The comparative values were similar in Groups I and V. Bax and 8-OHdG cell density were significantly elevated in Group II compared to Group I, Group IV and Group V. Probiotic bacteria were observed to have a protective effect against CP-induced hepatic damage.

Bu çalışmada Cyclophosphamide (CYP) uygulaması yapılan ratlarda karaciğer enzimleri (Aspartat aminotransferaz (AST), Alanin aminotransferaz (ALT), Alkalen fosfataz (ALP) ve histopatolojisi üzerine Naringin’in protektif etkilerinin araştırılması amaçlanmaktadır. Araştırmamızda yaklaşık 200-250 g ağırlığında, 40 adet erkek erişkin Sprague Dawley ırkı rat kullanıldı ve 5 grup oluşturuldu. Karaciğer enzimlerinin analizleri otoanalizörde ve spektrofotometrede yapıldı. Hematoksilen eosin ile boyanan karaciğer doku örnekleri ışık mikroskobunda incelendi. CYP’nin ratlarda hepatotoksiteye yol açtığı ve karaciğer enzimlerini artırdığı görüldü. AST, ALT ve ALP değerleri Kontrol grubunda 58±11, 32±8, 38±6; CYP grubunda 237±42, 168±44, 74±11; Naringin 50+CYP grubunda 223±33, 158±42, 62±9; Naringin 100+CYP grubunda 117±25, 107±24, 48±8; Naringin 100 grubunda ise 54±9, 31±7, 36±6 sırasıyla olarak bulundu. Kontrol grubundan elde edilen değerlere göre CYP verilen gruplarda ki AST, ALT ve ALP değerlerinin tamamında P<0.001 düzeyinde artış söz konusudur. CYP’nin karaciğer dokusunda oluşturduğu dejeneratif ve nekrotik doku hasarının Naringin’in etkisiyle dozlara bağlı olarak azaldığı saptandı. Sonuç olarak, Naringin’in farklı dozlarının, CYP ile indüklenen hepatotoksisitede protektif etkili olduğu belirlendi.

This study was carried out to determine vit. E, Se, vit. A, malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and ubiquinone-10 (CoQ10) levels and histopathological changes in sheep with white muscle disease (WMD). A total of 30 sheep were used; 20 sheep with WMD were brought to our clinic for diagnosis and treatment at various times, and 10 healthy sheep were in the control group. The Se, vit. E, vit. A, MDA, 8-OHdG, and CoQ10 values of the healthy and WMD sheep were as follows: 0.917 ± 0.037, 0.790 ± 0.067; 1.190 ± 0.011, 1.090 ± 0.021; 5.400 ± 0.275, 5.200 ± 0.173; 1.602 ± 0.264, 2.636 ± 0.576; 0.656 ± 0.197, 1.485 ± 0.271; and 0.280 ± 0.044, 1.753 ± 0.551 respectively (p < 0.05). According to histopathological and immunohistochemical findings in the WMD group, hyaline degeneration, Zenker's necrosis, and dystrophic calcification were observed in the muscle fibers. Immunohistochemically, 8-OHdG staining of the heart tissue determined a severe 8-OHdG expression in the WMD group. The findings of this study suggest that MDA, 8-OHdG, and CoQ10 values could be used as diagnostic and prognostic biomarkers in sheep affected with WMD.

In this study, it was aimed to investigate the protective effects of Naringin on nephrotoxicity by Cyclophosphamide

This study was carried out to determine the protective effects of lithium borate (LTB) on blood parameters and histopathological findings in experimentally induced acute cadmium (Cd) toxicity in rats. Twenty-eight male Wistar albino rats were used, weighing 200–220 g, and they were randomly divided into four groups, including one control and the following three experimental groups: a Cd group (0.025 mmol/kg), a LTB group (15 mg/kg/day orally for 5 days), and a LTB + Cd group (15 mg/kg/day orally for 5 days and Cd 0.025 mmol/kg by intraperitoneal injection on the fifth day). All the rats in the study were anesthetized with ketamine at the end of the sixth day, blood was taken from their hearts, and then the rats were decapitated. The values in the control and LTB group were usually close to each other. White blood cell (WBC), neutrophil %, and C-reactive protein (CRP) levels increased in the Cd and LTB + Cd groups while lymphocyte and monocyte levels decreased in a statistically significant manner, in comparison to the other groups. It was determined that the levels of red blood cells (RBCs), hematocrit (Htc), and hemoglobin (Hb) did not change in the groups. The levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the Cd and LTB + Cd groups significantly increased, in comparison to the other groups, while the glucose, alkaline phosphatase (ALP), albumin (ALB), and total protein (TP) levels decreased. According to histopathological findings in the control and LTB groups, the liver and kidney tissues were found to have normal histological structures. In the Cd group, severe necrotic hemorrhagic hepatitis, mild steatosis, and mononuclear cell infiltration were detected in the liver. In the LTB + Cd group, degeneration and mild mononuclear cell infiltration were found in the liver. Regarding the kidney tissue in the Cd group, severe intertubular hyperemia in both kidney cortex and medulla, as well as degeneration and necrosis in the tubulus epithelium, was observed. In the LTB + Cd group, mild interstitial hyperemia and mononuclear cell infiltration was detected. Resultantly, it can be said that LTB at this dose has non-toxic effects and some beneficial effects for liver and kidney damage caused by acute Cd toxicity.

Bu çalışmada, ratlarda Cyclophosphamide (CP) ile indüklenen hemorajik sistitte izole mesane düz kas kontraksiyonları ve mesane histopatolojisi üzerine Rutin’in etkileri araştırıldı. Çalışmada 24 adet erişkin dişi Sprague Dawley rat kullanıldı ve ratların ağırlıkları ortalama 200-250 gramdı. Dört deney grubu oluşturuldu ve her bir grupta 6 rat vardı. Kontrol ve CP grubuna 7 gün intraperitoneal (ip) serum fizyolojik uygulandı. Ayrıca, CP grubuna serum fizyolojik uygulamasının 5. günü tek doz CP (150 mg/kg, ip) enjekte edildi. Rutin uygulanan gruplara serum fizyolojikte çözdürülmüş Rutin (50 mg/kg, ip) 7 gün enjekte edildi. Rutin+CP grubuna, Rutin uygulamasının 5. günü tek doz CP uygulandı. Deneysel uygulamanın 8. günü ratlar anestezi eşliğinde dekapite edilerek mesaneleri izole edildi. İzole mesane düz kas şeritlerinde Asetilkolin (Ach) (10-4 M) ve Potasyum Klorür (KCI) (60 mM) ile indüklenen kontraksiyon değerleri elde edildi. Ayrıca mesaneler hematoksilen eozin ile boyanarak histopatolojik değerlendirme yapıldı. CP grubundaki ratlarda ACh ve KCl ile indüklenen in vitro kontraksiyonların arttığı fakat istatistiksel önem arz etmediği (P>0.05) ve Rutin uygulamasının artan kontraksiyon cevaplarını azalttığı belirlendi. Histopatolojik incelemede mesane lümeninde epitel döküntü, mukoza epitelinde deskuamasyon, koagulasyon nekrozu ve şiddetli düzeyde eritrosit görülürken, Rutin’in bu değişiklikleri azalttığı görüldü. Sonuç olarak; CP ile indüklenen hemorajik sistitte mesane kontraktilitesi ve histopatolojisi üzerine Rutin uygulamasının protektif etkili olduğu belirlendi.