Rutin ameliorates cisplatin‐induced reproductive damage via suppression of oxidative stress and apoptosis in adult male rats

Cisplatin (CP) treatment causes damage in the male reproductive system. Rutin (RUT) is a naturally occurring flavonoid glycoside that has antioxidant and anti‐inflammatory properties. This study aimed to investigate effects of RUT against cisplatin‐induced reproductive toxicity in male rats. Twenty‐one adult male Sprague Dawley rats were used. The control group received physiological saline with oral gavage during 14 days, and physiological saline was injected intraperitoneally (IP) in 10th days of study. CP Group received physiological saline during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. RUT + CP group received RUT (150 mg kg^?1) during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. Spermatological parameters (including motility, cauda epididymal sperm density, dead sperm percentage and morphological sperm abnormalities), biochemical (MDA, GSH, GSH‐px, SOD and CAT), histological (H&E dye) and immunochemistry evaluations of testicles were evaluated. CP treatment caused damage on some spermatological parameters, increased the oxidative stress and induced testicular degeneration and apoptosis when compared to the control group. However, RUT treatment mitigates these side effects when compared to the CP alone group. IT is concluded that RUT treatment may reduce CP‐induced reproductive toxicity as a potential antioxidant compound.     

The preventive role of wheat germ oil against sertraline‐induced testicular damage in male albino rats

Sertraline is an antidepressant medication used extensively in the therapy of depression. The present investigation was intended to estimate the actual protective role of wheat germ oil on sertraline‐caused testicular injury in albino rats. Sertraline (human therapeutic dose, 15.63 mg/kg) was orally administrated to rats for 28 successive days. Sertraline‐administered rats were concurrently supplemented with wheat germ oil (human therapeutic dose, 68.75 mg/kg) for 28 successive days. Sertraline administration induced an elevation in testicular DNA damage and acute testicular damage illustrated by the histopathological alterations including marked degeneration and necrosis of germ cells lining seminiferous tubules, as well as interstitial oedema, congestion of interstitial blood vessel. Wheat germ oil administration potentially mitigated the histopathological alterations of sertraline‐administered rats. Lipid peroxidation, oxidative stress biomarker, showed a significant elevation in testicular tissue of sertraline‐administered rats. Furthermore, glutathione content and catalase activity were decreased in testicular tissue of sertraline‐administered rats. Serum testosterone level was elevated in sertraline‐administered rats. Wheat germ oil significantly reduced lipid peroxidation of testicular tissue and improved the antioxidant defences. Finally, wheat germ oil has a preventive role against testicular damage induced by sertraline in rats probably via its potential to prevent reactive oxygen species.     

Carob attenuates nicotine-induced oxidative stress and intratesticular damage in male rats

In this study, we aimed to evaluate the effect of carob extract against intratesticular histological, apoptotic, biochemical and spermatogenic changes in rats exposed to nicotine. Twenty-eight rats were divided into four groups and were administered saline, nicotine, carob, or nicotine + carob once a day for 35 days. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), GSH, total anti-oxidative status (TAS), total oxidative status (TOS), oxidative stress index (OSI), IL-6, TNF-α and seminal parameters were evaluated. Johnsen's testicular histopathological examination, factor VIII protein (angiogenesis marker) and the number of apoptotic cells were determined in the testicular tissues. The spermatogenic and histopathological examination revealed that nicotine + carob group had significant positive changes in seminal parameters, Johnsen score, apoptotic cell count and factor VIII protein compared to nicotine group. Biochemical test results indicated that the nicotine + carob group had significantly lower TAS levels compared to the control group; however, those levels were higher than those of the nicotine group. Nicotine caused a significant increase in IL-6 and TNF-α levels compared to the control group, but carob seems to significantly counteract that increase. In conclusion, carob extract had positive effects on spermatogenesis and reduced testicular parenchymal damage, apoptosis and angiogenesis.     

Black soot exposure induced hypothalamic and testicular oxidative stress and apoptosis in male rats

Air pollution constitutes the largest cause of environmental risks today. At present, no scientific publication linking environmental black soot and derangement in the hypothalamus and testis of rats exists. This study investigated the effect of black soot exposure on hypothalamic and testicular functions of male rats exposed to black soot for 4, 8 and 12 weeks respectively. The hypothalamus and testis were processed for biochemical analysis. Results show that black soot exposure for 4, 8 and 12 weeks significantly (p < .05) increased oxidative stress markers both in the testis and in the hypothalamus of rats. Also, black soot exposure significantly (p < .05) decreased the alkaline phosphatase, acid phosphatase as well as lactate dehydrogenase activities in the testis. Furthermore, the result demonstrated an upregulation of the protein expression of caspase-3, an indication of increased apoptosis which led to the disruption of the histological architecture of the hypothalamus and testis. Taken together, black soot exposure induced hypothalamic and testicular oxidative stress and apoptosis in male rats.     

Testicular gametogenic and steroidogenic activities in chlorpyrifos insecticide-treated rats: a correlation study with testicular oxidative stress and role of antioxidant enzyme defence systems in Sprague-Dawley rats

The present works examined an adverse effect of chlorpyrifos insecticide on testes and lipid peroxidation at low doses (5 mg-10 mg kg(-1) body weight) and the role of antioxidant enzymes systems at higher doses (20-30 mg kg(-1) body weight) in albino rats. At low doses, reduction in plasma levels of testosterone and FSH and LH hormones along with the significant shrinkage of seminiferous tubules and gametogenic changes in germ cells were noticed. But these changes were restored with the revival of serum testosterone, FSH and LH along with regression of testis at higher doses. Similarly, level of testicular lipid peroxidation was elevated, whereas levels of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and steroidogenic enzymes activities (Δ(5) , 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase) were reduced significantly at low doses. But, rat testes showed a significant decrease in lipid peroxidation and concomitant increase in antioxidant enzymes and steroidogenic enzymes activities at higher doses. Results showed that at higher doses of chlorpyrifos treatments, rat testes were shown to trigger their natural defence mechanism which became operative possibly through corrective measure of synthesis of antioxidant defence enzymes and steroidogenic enzymes and pituitary gonadotrophins hormone feedback mechanisms.     

Oxidative stress, DNA damage and apoptosis in male infertility: a clinical approach

OBJECTIVE: To characterize the clinical outcomes of androgen deprivation therapy (ADT) as the sole therapy for localized prostate cancer, and to determine independent predictors of disease progression, as recent studies indicate an increasing use of ADT. PATIENTS AND METHODS: The records of all patients with cT1-4NXM0 adenocarcinoma of the prostate treated with ADT as the primary initial therapy at the Portland Veterans Affairs Medical Center between 1993 and 2000 were reviewed. Age, race, Charlson Health Index, family history, prostate-specific antigen (PSA) level, PSA density, digital rectal examination (DRE) findings, Gleason score, and percentage of positive biopsy cores at diagnosis were recorded for 81 patients. Patients had a median (SD, range) age of 73 (5.6, 58-84) years, a PSA level of 14.3 (34.6, 1.4-252) ng/mL and tumours were classified as Gleason score < or = 5 in 9% of patients, 6 in 31%, 7 in 31% and 8-10 in 30%. Outcomes extracted were PSA progression, PSA nadir, bone fractures, local progression, distant progression and overall survival. RESULTS: With a median (range) follow-up of 54 (6-115) months, the incidence of local progression, distant progression, bone fractures, PSA progression, and death were 10%, 7%, 25%, 21% and 41% respectively. The percentage of positive biopsy cores > or = 83%, age < 70 years, Gleason score > or = 7, abnormal DRE, and PSA nadir > or = 0.2 ng/mL were significantly associated with PSA progression by univariate analysis. The multivariate analysis identified age < 70 years (hazard ratio 6.52, 95% confidence interval 2.29-18.55) and Gleason score > or = 6 (4.0, 2.0-12.0) as independent risk factors for PSA progression. CONCLUSIONS: ADT resulted in modest control of localized prostate cancer, but younger patients and those with Gleason > or = 6 cancers were at higher risk of treatment failure. Toxicity, principally in the form of bone fractures, was high.     

Quercetin ameliorates methotrexate-induced renal damage,apoptosis and oxidative stress in rats

Abstract

Background: In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined. Materials and methods: A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX?+?QE group. Rats in MTX group received 20?mg/kg of single dose of MTX, while those in MTX?+?QE group received 20?mg/kg of single dose MTX, in addition to 15?mg/kg of QE administered 30?min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments. Results: Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX?+?QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration. Conclusions: In conclusion, renal toxic effects of MTX may be alleviated by QE.     

Mitigation of paracetamol‐induced reproductive damage by chrysin in male rats via reducing oxidative stress

Paracetamol (PRC) is a nonsteroidal anti‐inflammatory drug used widely as a painkiller for various diseases and as the symptomatic flu cure in several countries worldwide. PRC toxicity may occur under conditions of the overdose usage. Chrysin (CR) is a flavonoid that is naturally present in several plants, honey and propolis. The aim of this study was to investigate the effects of CR (at the doses of 25 mg kg⁻¹ and 50 mg kg⁻¹) pre‐treatment over seven consecutive days against PRC‐induced reproductive toxicity in male rats. Our results showed that PRC toxicity decreased the sperm motility, and increased dead sperm rate, abnormal sperm cell rate, apoptosis and MDA levels in testicular tissues. Pre‐treatment with CR at the dose of 25 and 50 mg kg⁻¹ for 7 days mitigated side effects of acute PRC toxicity in male reproductive system proportionally in a dose‐dependent manner. This possible protection mechanism might be dependent on the antioxidant activity of CR. In conclusion, pre‐treatment with CR at the dose of 25 and 50 mg kg⁻¹ for 7 days can be the beneficial against PRC‐induced reproductive toxicity proportionally in a dose‐dependent manner.     

Investigating the protective effect of aerobic exercise on oxidative stress and histological damages of testicular tissue associated with chlorpyrifos in male rats

The current study aimed to investigate the protective effects of moderate aerobic exercise against chlorpyrifos (CPF)-induced testes dysfunction. In excremental study, 48 adult male albino rats were randomly allocated into 16 groups of 3 rats each. Twelve experimental groups received intraperitoneal injection (5 days a week) of either 1.0 or 3.0 mg/kg body weight CPF in DMSO for 2, 4 or 6 consecutive weeks. Seven of these experimental groups were subjected to run at moderate exercise intensity for 5 days per week over 2 weeks, whereas the other groups were not. Two groups (sham groups) were administered to the equal volume of vehicle (DMSO) for 4 or 6 consecutive weeks. The remaining two groups comprised the control groups including a sedentary and an exercise-trained control group. Exercise training leads to a markedly increase in testicular superoxide dismutase (SOD) activity in CPF-exposed rats compared with corresponding sedentary animals (p < .05). Lipid peroxidation level was found to be significantly decreased in the testis of exercised animals that had been exposed to CPF (p < .05). Our results suggest that aerobic exercise can alleviate the oxidative stress induced by sub-acute CPF exposure in testis. Exercise training could barely mitigate CPF-induced testicular damages in rats.     

Melatonin prevents gentamicin‐induced testicular toxicity and oxidative stress in rats

This study investigated the protective effects of melatonin (MT) against gentamicin (GM)‐induced testicular toxicity and oxidative damage in rats. GM (100 mg kg^?1) was injected intraperitoneally (i.p.) to rats for 6 days. MT (15 mg kg^?1) was administered i.p. to rats for 6 days at 1 hr after the GM treatment. GM caused a decrease in prostate and seminal vesicle weights, sperm count and sperm motility. Histopathological examination showed various morphological alterations in the testis, characterised by degeneration of spermatogonia/spermatocytes, decrease in the number of early spermatogenic cells and vacuolisation. In addition, an increased malondialdehyde concentration and decreased glutathione content and glutathione reductase, catalase and glutathione‐S‐transferase activities were found in the testis. In contrast, MT treatment significantly attenuated the testicular toxicity of GM, including decreased reproductive organ weights, sperm count, and sperm motility and increased histopathological alterations. MT also had an antioxidant benefit by decreasing the lipid peroxidative product malondialdehyde and increasing the level of the antioxidant glutathione and the activities of antioxidant enzymes in the testis. These results indicate that MT prevents testicular toxicity induced by GM in rats, presumably due to its potent antioxidant activity, and its ability to inhibit lipid peroxidation, and restore antioxidant enzyme activity.     

Protective effect of rutin on mercuric chloride-induced reproductive damage in male rats

This study investigated the effects of rutin against reproductive damage caused by toxic mercury in male rats. Thirty-five Sprague Dawley rats were used. Control group was injected with saline for 7 days. The rutin-100 group received 100 mg/kg/b.w. rutin for 7 days. Mercuric chloride (HgCl₂) group received 1.23 mg/kg/b.w. of HgCl₂ for 7 days. Mercury chloride + rutin-50 group received 50 mg/kg/b.w. rutin and HgCl₂ 1.23 mg/kg/b.w. for 7 days. HgCl₂ + rutin-100 group received 100 mg/kg/b.w. rutin and HgCl₂ 1.23 mg/kg/b.w. for 7 days. It was detected that HgCl₂ treatment increased malondialdehyde (MDA) levels, tumour necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) expressions, necrosis and degeneration of spermatogonium, dead and abnormal sperm percentages; tubular walls thinning; and decreased antioxidant enzyme activities and sperm motility. It was determined that rutin application reduced testicular damage caused by HgCl₂. In conclusion, rutin administration may treat HgCl₂ toxicity in testes.     

Achillea millefolium alleviates testicular damage in paclitaxel-intoxicated rats via attenuation of testicular oxido-inflammatory stress and apoptotic responses

The aim of this study was to investigate the effects of Achillea millefolium extract in paclitaxel-induced testicular toxicity in rats. The groups were designed as (1) control, (2) paclitaxel (8 mg/kg, intraperitoneally), (3) paclitaxel (8 mg/kg, intraperitoneally) + Achillea millefolium (200 mg/kg, orally for 14 consecutive days) and (4) paclitaxel (8 mg/kg, intraperitoneally) + Achillea millefolium (400 mg/kg, orally for 14 consecutive days). Serum levels of testosterone, luteinising hormone and follicle-stimulating hormone, as well as total antioxidant capacity and total oxidant status were measured one day after receiving the last dose of Achillea millefolium extract. Testicular superoxide dismutase activity, malondialdehyde, tumour necrosis factor alpha and interleukin-1β levels, the expressions of nuclear factor kappa B and caspase-3 were evaluated. In addition, testicular sections were evaluated histopathologically and 8-hydroxy-2′-deoxyguanosine was detected immunohistochemically. Achillea millefolium improved the levels of luteinising hormone, follicle-stimulating hormone and testosterone, upregulated testicular antioxidant enzymes and downregulated inflammation. Furthermore, we observed that Achillea millefolium restored testicular histopathological structure and significantly suppressed oxidative DNA damage and apoptosis by reducing the expression of caspase-3. Taken together, our results suggest that Achillea millefolium has protective effects against paclitaxel-induced testicular toxicity and is a promising natural product with the potential to improve male fertility.     

Selenium attenuates venlafaxine hydrochloride-induced testicular damage in mice via modulating oxidative stress and apoptosis

The present study assessed the effect of selenium (Se) supplementation on Venlafaxine hydrochloride (VH)-induced testicular toxicity. Mice were segregated into Group I (C), Group II (0.5 ppm Se), Group III (VH at a dose 60 mg/kg b.w.) and Group IV (Se was given as per Group II, and VH was given as per Group III). After 10 weeks, sperm parameters, histology, sperm cell counts, antioxidants activities, apoptotic proteins and molecular analysis of testicular tissue were evaluated. Group III had significantly lower sperm concentration (from 2.17 ± 0.28 to 1.04 ± 0.22) and sperm motility (from 68.04 ± 5.5 to 21.47 ± 5.21), and showed an extensive vacuolisation in the germinal epithelium, abnormal basement membrane, and reduced germ cell number as compared to Group I. However, selenium supplementation in Group IV substantially increased sperm concentration (1.47 ± 0.48) and motility (33.27 ± 8.66), improved the histoarchitecture and repopulated the germ cells as observed by raised numbers of spermatogonia, spermatocytes, round spermatids and elongated spermatids contrasted to Group III. Group IV also showed a noteworthy decreased ROS, LPO levels, as well as expressions of Bax, caspase-9, and caspase-3 and increased the SOD, CAT, GPx, and GSH activities as well the expression of Bcl-2 as compared to Group III. This effect was further supported by FTIR analysis for nucleic acids. Thus, selenium supplementation showed significant protection against VH-induced testicular toxicity.     

氧化应激损伤在男性不育症中的影响

造成精子数量、质量及生殖机能下降的原因十分复杂。随着自由基理论的建立和发展,研究者们逐渐发现活性氧介导的氧化应激对精子的损伤作用可能是男性不育的发病原因之一。本文将对氧化应激损伤在男性不育症中的影响进行阐述。     

Protective effect of alpha glucosyl hesperidin (G‐hesperidin) on chronic vanadium induced testicular toxicity and sperm nuclear DNA damage in male Sprague Dawley rats

The study was conducted to evaluate the vanadium‐induced testicular toxicity and its effect on sperm parameters, sperm nuclear DNA damage and histological alterations in Sprague Dawley rats and to assess the protective effect of G‐hesperidin against this damage. Treatment of rats with vanadium at a dose of 1 mg kg bw^?1 for 90 days resulted in significant reduction in serum testosterone levels, sperm count and motility. Further, a parallel increase in abnormal sperm morphology and adverse histopathological changes in testis was also associated with vanadium administration when compared to normal control. Moreover, sperm chromatin dispersion assay revealed that vanadium induces sperm nuclear DNA fragmentation. A marked increase in testicular malondialdehyde levels and decreased activity of antioxidant enzymes such as superoxide dismutase and catalase indicates vanadium‐induced oxidative stress. Co‐administration of G‐hesperidin at a dose of 25 and 50 mg kg bw^?1 significantly attenuated the sperm parameters and histological changes by restoring the antioxidant levels in rat testis. These results suggested that vanadium exposure caused reduced bioavailability of androgens to the tissue and increased free radical formation, thereby causing structural and functional changes in spermatozoa. G‐hesperidin exhibited antioxidant effect by protecting the rat testis against vanadium‐induced oxidative damage, further ensures antioxidant potential of bioflavonoids.     

Effect of food restriction on ghrelin in adult male rats and its relation to male reproductive hormones

Ghrelin is an endogenous ligand for growth hormone secretagogue (GHS) receptor (GHS‐R). It has recently emerged as an orexigenic food intake controlling signal acting upon hypothalamic centres. To study the effect of food restriction on ghrelin level and its relation to male reproductive hormones, 32 adult male albino rats divided into two groups: Group I (8 rats as a control group) fed ad libitum for 21 days and 24 rats as Group II (food‐restricted group) fed 30% of ad libitum intake of food consumed by the control group. Rats were weighed every 3 days. Group II rats were further subdivided into three subgroups: IIa, IIb and IIc that were killed at days 8, 16 and 21 from the start of food restriction respectively. Ghrelin level was assayed by ELISA technique in serum samples and tissue homogenates prepared from the stomach and hypothalamus. In addition, male reproductive hormones: testosterone, follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) were assayed in serum by chemiluminescence. Mean body weight of food restricted rats was observed to decrease during the period of the experiment. Food restriction produced a significant increase of serum ghrelin and a significant decrease of both gastric and hypothalamic ghrelin in group II when compared with group I. The changes in ghrelin level varied with the duration of food restriction. Significant inverse correlation was found between serum ghrelin and each of gastric and hypothalamic ghrelin in group II. A significant decrease of testosterone, FSH and LH were found in food restricted rats compared with controls. The decrease was significantly related to the duration of food restriction. Significant inverse correlation was detected between serum ghrelin and each of the male reproductive hormones in food restricted group II rats. Thus ghrelin could be one of the hormones responsible for the suppression of male reproductive axis in case of negative energy balance.     

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress,inflammatory responses and apoptosis

Background: The aim of this study was to assess the preventive effect of xuezhikang (XZK) to replace atorvastatin on the contrast media-induced acute kidney injury (CI-AKI).

Methods: The male Sprague–Dawley rats were divided into five groups: group 1 (sham), injected with normal saline; group 2 (XZK), treated with XZK; group 3 contrast media (CM), injected with CM; group 4 (CM?+?ATO), injected with CM?+?pretreatment with atorvastatin; group 5 (CM?+?XZK), injected with CM?+?pretreatment with XZK. Twenty-four hours after injection with normal saline or CM, the blood sample and the kidneys were collected for the measurement of biochemical parameters, oxidative stress markers, nitric oxide production, inflammatory parameters, as well as renal histopathology and apoptosis detection.

Results: Our results indicated that XZK restored the renal function by reducing serum blood urea nitrogen (BUN) and serum creatinine (Scr), depressing renal malondialdehyde (MDA), increasing renal NO production, decreasing TNF-ɑ and IL-6 expression, attenuating renal pathological changes and inhibiting the apoptosis of renal tubular cells.

Conclusion: XZK’s therapeutic effect is similar, or even better than atorvastatin at the same effectual dose in some parts.     

Sitagliptin protects male albino rats with testicular ischaemia/reperfusion damage: Modulation of VCAM-1 and VEGF-A

Twisting of the spermatic cord is considered a popular problem in the urological field, which may lead to testicular necrosis and male infertility. Sitagliptin, a glucose-lowering agent, proved to have a vindicatory function in myocardial and renal ischaemia/reperfusion (I/R), but its role in testicular I/R has not yet been studied. The current work investigates its capability to recover the testicular I/R injury with shedding more light on the mechanism of its action. Four groups were used: sham, sham pretreated with sitagliptin, I/R and sitagliptin/I/R-pretreated groups. The outcomes proved that I/R significantly decreased the serum testosterone, with a major increase in oxidative, inflammatory and nitrosative stress, along with a reduction in testicular vascular endothelial growth factor-A level with marked germinal cell apoptosis. However, pretreatment with sitagliptin significantly reversed the profound testicular I/R damaging effects, on the basis of its antioxidant, anti-inflammatory and anti-apoptotic activities with the ability of recuperation of the testicular vascularity.     

Rutin attenuates gentamicin-induced renal damage by reducing oxidative stress,inflammation, apoptosis,and autophagy in rats

Abstract

Gentamicin is commonly used against gram-negative microorganisms. Its therapeutic use is mainly limited by nephrotoxicity. This study was aimed at evaluating the effect of rutin on oxidative stress, inflammation, apoptosis, and autophagy in gentamicin-induced nephrotoxicity in rats. The rats were treated with saline intraperitoneally (group I), 150?mg/kg of rutin orally (group II), 80?mg/kg of gentamicin intraperitoneally for 8?d (group III), or 150?mg/kg of rutin plus 80?mg/kg of gentamicin (group IV). The serum urea, creatinine, kidney malondialdehyde (MDA), and reduced glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and protein concentration were measured, and renal histopathology analysis and immunohistochemical staining were performed. Rutin pretreatment attenuated nephrotoxicity induced by gentamicin by reducing the urea, creatinine, and MDA levels and increasing the SOD, CAT, and GPx activity, and the GSH levels. The rutin also inhibited inducible nitric oxide synthase (iNOS), cleaved caspase-3 and light chain 3B (LC3B), as evidenced by immunohistochemical staining. The present study demonstrates that rutin exhibits antioxidant, anti-inflammatory, anti-apoptotic, and anti-autophagic effects and that it attenuates gentamicin-induced nephrotoxicity in rats.