姜黄素对糖尿病大鼠疼痛过敏的影响

目的：神经病理性痛是糖尿病最常见的并发症之一,本课题旨在探讨姜黄素对糖尿病大鼠痛觉过敏的影响及其分子机制。方法：30只雄性SD大鼠随机分为对照组、糖尿病组和姜黄素治疗纽,模型纽和姜黄素治疗组利用腹腔注射链脲佐菌素（Streptozotocin,STZ）制备大鼠糖尿病模型,定期检测大鼠血糖、饮食、体重等变化,治疗组于STZ注射2wk后定期灌服姜黄素,分别在2wk和4wk后检测各组大鼠热痛敏和机械痛敏反应,在第4wk利用ELISA分别检测各组大鼠脊髓背角TNF-α表达变化。结果：STZ注射组大鼠2周后出现血糖〉14mol／L,并且该模型具有高血糖、体重增长缓慢、多饮多食多尿的特点,符合Ⅰ型糖尿病特征,痛行为测试结果显示糖尿病大鼠出现痛觉过敏,经过给予姜黄素灌服治疗后,痛觉过敏有所减轻,ELISA分析结果表明糖尿病大鼠脊髓背角TNF-α表达升高,经过姜黄素治疗后TNF-α表达有所下降。结论：成功制备STZ-型糖尿病大鼠模型,经过姜黄素治疗可以减轻糖尿病引起的疼痛过敏,姜黄素对糖尿病疼痛的治疗作用可能是通过降低大鼠脊髓背角TNF-α表达实现的。     

Postacute Effects of Kisspeptin‐10 on Neuronal Injury Induced by l‐Methionine in Rats

Apart from its effect on the regulation of reproductive function, recent studies indicate that kisspeptin may play roles in the antioxidant defense system. The antioxidant defense system and oxidative stress contribute to the etiology and pathogenesis of neuronal cell death after brain injury. We have investigated the postacute effect of kisspeptin‐10 on brain injury induced by l ‐methionine. DNA fragmentation, malondialdehyde (MDA), reduced glutathione levels, and superoxide dismutase (SOD) activities were analyzed. Our results showed that methionine treatment increases apoptotic cell death. Kisspeptin alone showed no side effect on apoptotic cell death. However, kisspeptin treatment reversed the proapoptotic effect of methionine associated with reduced MDA and increased glutathione levels. Furthermore, SOD activity was completely depleted in methionine‐treated animals. In conclusion, our results revealed that delayed kisspeptin‐10 treatment reduces neuronal cell death by activation of SOD activity.     

Impact of Acute Streptozotocin‐Induced Diabetes on ABC Transporter Expression in Rats

Hepatic ABC efflux transporters control the cellular uptake (in basolateral membranes) and excretion (in apical membranes) of many substrates. Since type‐1 diabetes mellitus (T1DM) is associated with altered hepatobiliary excretion of many endogenous and exogenous substances, we examined key hepatic ABC transporters and levels of the endogenous substrate glutathione in rats with acute streptozotocin‐induced T1DM. Renal transporters and inflammatory markers were also examined. Abcb1, Abcc1–4, and Abcg2 were measured using qRT‐PCR. Glutathione was measured in liver tissue, plasma, and urine. Inflammatory markers, including C‐reactive protein (CRP), were measured in plasma via ELISA. In diabetic rats, Abcb1a, Abcc2, and Abcg2 (apical) were decreased, while Abcc4 (basolateral) was increased. Abcb1a and Abcc2 inversely correlated with plasma CRP. Diabetic and control rats exhibited similar hepatic glutathione, but levels in diabetic plasma were lower. When standardized to urinary output, diabetic rats excreted 6.7‐fold more glutathione in urine than controls. Renal transporter levels were normal in diabetic rats. Results show apical transporters involved in hepatobiliary excretion are downregulated in T1DM, possibly through an inflammation‐mediated process. Findings suggest that there may be a vectorial shift from hepatic to renal excretion for some substrates in T1DM.     

Antihyperlipidemic Effect of Fisetin,a Bioflavonoid of Strawberries,Studied in Streptozotocin‐Induced Diabetic Rats

Chronic hyperglycemia in diabetes is associated with profound changes in lipid and lipoprotein metabolism, with resultant alterations in particle distribution within lipoprotein classes. In the present study, an attempt has been made to explore the antihyperlipidemic effect of fisetin in streptozotocin‐induced experimental diabetes in rats. Upon fisetin treatment to diabetic rats, the levels of blood glucose were significantly reduced with an improvement in plasma insulin. The increased levels of lipid contents in serum, hepatic, and renal tissues observed in diabetic rats were normalized upon fisetin administration. Also, the decreased levels of high‐density lipoprotein cholesterol, and increased levels of low‐density lipoprotein (LDL) and very LDL (VLDL) cholesterol in serum of diabetic rats were normalized. Oil Red O staining established a large number of intracellular lipid droplets accumulation in the diabetic rats. Fisetin treatment exacerbated the degree of lipid accumulation. The results of the present study exemplify the antihyperlipidemic property of the fisetin.     

Ameliorative Effect of Carvacrol on Cisplatin‐Induced Reproductive Damage in Male Rats

Cisplatin (CP) treatment causes the damage in male reproductive system. Carvacrol (CARV) is an antioxidant that is naturally found in some plants. We aimed to investigate the effect of CARV on CP‐induced reproductive toxicity in male rats. Eighteen adult male Sprague–Dawley rats were used. The control group (n = 6) was treated orally with physiological saline (PS) daily for 14 days and a single intraperitoneal (IP) PS injection on day 10. The CP group (n = 6) was administered with daily oral PS for 14 days and a single IP injection of 10 mg/kg CP on day 10. The CARV + CP group (n = 6) was treated with daily 75 mg/kg oral CARV for 14 days and a single IP injection of 10 mg/kg CP on day 10. CP treatment caused the damage on some spermatological parameters (motility, live sperm rate, and abnormal sperm rate), increased the oxidative stress, and induced testicular degeneration and apoptosis. However, CARV treatment mitigates CP‐induced reproductive toxicity.     

Oxidative Stress and Hepatocellular Injury Induced by Oral Administration of Cr3+ in Chicken

This study aims to investigate the oxidative stress and hepatocellular injury induced by Cr³⁺ in chicken. Different doses of CrCl₃ solutions (50% LD₅₀, 25% LD₅₀, and 12.5% LD₅₀) and equivalent water were orally administered to chicken. Chicken liver samples were measured for the activities of antioxidant enzymes, the contents of glutathione, total antioxidant capacity (T‐AOC), malondialdehyde (MDA), and hydrogen peroxide to indirectly evaluate the oxidative stress in chicken liver. Results indicated that the oral administration of Cr³⁺ at high dose significantly increased (P < 0.05) the MDA levels after 28 days of exposure, with decreased T‐AOC, glutathione, and antioxidant enzymes activities. Low and medium doses groups show that T‐AOC, glutathione, and antioxidant enzymes activities increased after 14 days, then decreased gradually, but low and medium groups higher than control group, only high group lower than control group finally. These statistics and histopathological analysis suggest that high dose and long‐term exposure of Cr³⁺ induce oxidative stress and hepatocellular injury.     

姜黄素对双酚A致小鼠卵巢氧化损伤的保护

本文旨在研究姜黄素(CRC)对双酚A(BPA)诱导的小鼠卵巢氧化损伤的保护作用。将28日龄雌性小鼠分为对照组、姜黄素组、双酚A组和双酚A加姜黄素组,连续灌胃6周。收集卵巢,通过活性氧(ROS)水平的检测、卵巢闭锁卵泡的观察以及3种关键抗氧化酶表达和活性的测定,研究姜黄素对双酚A诱发的卵巢氧化损伤的保护作用及机制。结果显示,与对照组相比,双酚A暴露后明显增加了卵巢的活性氧水平,造成氧化应激,提高了卵巢中有腔卵泡闭锁比例。与双酚A组相比,双酚A和姜黄素共同处理组降低了卵巢的活性氧水平和卵巢中有腔卵泡闭锁比例。双酚A暴露降低了卵巢超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)以及过氧化氢酶(CAT)的表达和活性,姜黄素逆转了双酚A诱导的3种抗氧化酶表达和活性的下降。结果表明,姜黄素可逆转双酚A通过氧化应激造成的卵巢损伤。     

Cisplatin‐Induced Testicular Toxicity in Rats: The Protective Effect of Arjunolic Acid

In the present study, the effect of arjunolic acid on testicular damage induced by intraperitoneal injection of rats with 7 mg/kg cisplatin was studied. Cisplatin induced a significant reduction in testicular weights, plasma testosterone, and testicular reduced glutathione levels in addition to a significant elevation of testicular malondialdehyde levels and testicular gene expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor‐α (TNF‐α), and p38 mitogen‐activated protein kinase (MAPK) when compared with the control group (p < 0.05). Lower tubular diameters and depletion of germ cells and irregular small seminiferous tubules with Sertoli cells only were observed in the cisplatin group. Arjunolic acid administration significantly corrected the changes in both biochemical and histopathological parameters. Arjunolic acid plays a significant protective role against cisplatin‐induced testicular injury by attenuating oxidative stress parameters along with downregulation of iNOS, TNF‐α, and p38‐MAPK testicular expressions.     

Protection by Edaravone,a Radical Scavenger,against Manganese‐Induced Neurotoxicity in Rats

Manganese (Mn) is a required element for biological systems; however, its excessive exposure may lead to a neurological syndrome known as manganism. The aim of the present study was to assess the toxic effects of subacute exposure of Mn by measuring weight gain, motor performance, and biochemical parameters (complex I activity, lipid peroxides, and protein carbonyls) in brain mitochondria in rats. We also examined whether edaravone (EDA), a radical scavenger, exerts protective effects against Mn‐induced neurotoxicity. In addition, we evaluated the accumulation of Mn in brain regions using magnetic resonance imaging. Mn‐exposed rats revealed significantly impaired motor performance, weight loss, and Mn accumulation in particular brain area. Lipid peroxides and protein carbonyls were significantly increased in Mn‐exposed rats, whereas complex I activity was found to be decreased. EDA treatment significantly prevented mitochondrial oxidative damage and improved motor performance. These findings suggested that EDA might serve as a clinically effective agent against Mn‐induced neurotoxicity.     

Age‐Related Changes in Fatty Acids in Obese Offspring of Streptozotocin‐Induced Diabetic Rats

Objective: The long‐term effects of fetal hyperinsulinemia, time course of changes in liver and very‐low‐density lipoprotein (VLDL) lipid levels and fatty acid compositions were investigated in obese offspring of streptozotocin‐induced mildly diabetic rats. Research Methods and Procedures: Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. Liver and VLDL lipids and fatty acids were analyzed in offspring at different ages. Results: At birth, obese pups had higher VLDL triglyceride levels, saturated fatty acids, and C20:4n‐6. They also had lower C18:2n‐6 proportions in VLDL triglycerides, phospholipids, and cholesteryl esters than controls pups. In 1‐month‐old male and female obese rats, VLDL and liver lipid amounts were similar to those in their respective controls; however, high levels of C18:2n‐6 and C20:4n‐6 were noted in liver and VLDL lipids. At the age of 2 months, liver and VLDL triglyceride levels were higher in obese females than in control females. Fatty acid abnormalities seen in obese rats included low C18:3n‐3 and high C22:6n‐3 proportions in liver triglycerides and phospholipids. At the age of 3 months, obese rats, both males and females, compared with control animals, had higher VLDL and hepatic lipids with reduced C20:4n‐6 levels and polyunsaturated/saturated fatty acids ratios in hepatic and VLDL triglycerides and phospholipids. Discussion: Fetal obesity, associated with alterations in VLDL lipid fatty acid composition, represents an important risk factor for adult obesity and diabetes.     

Netrin‐1 Pretreatment Protects Rat Kidney against Ischemia/Reperfusion Injury via Suppression of Oxidative Stress and Neuropeptide Y Expression

Netrin‐1 has been found to protect kidneys from ischemia/reperfusion injury. In this study, we aimed to address whether the protective effects were mediated through suppression of oxidative stress and neuropeptide Y. Compared to sham‐operated animals, animals after ischemia/reperfusion showed marked kidney damage and significantly increased levels of serum creatinine, blood urea nitrogen, malondialdehyde, and neuropeptide Y. Renal myeloperoxidase activity was elevated in animals with ischemia/reperfusion relative to sham‐operated animals, whereas renal superoxide dismutase activity was reduced. Netrin‐1 pretreatment attenuated ischemia/reperfusion‐induced functional and pathological changes in the kidney. Moreover, the ischemia/reperfusion‐induced changes in the oxidative stress biomarkers and neuropeptide Y were significantly counteracted by prior administration of netrin‐1. Taken together, our data showed that netrin‐1 pretreatment prevented renal ischemia/reperfusion injury, at least partially through reduction of oxidative stress and neuropeptide Y expression. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:231‐236, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21474     

不同天数姜黄素灌胃对顺铂所致小鼠胃排空障碍的作用

目的:探讨不同天数姜黄素灌胃对顺铂所致小鼠胃排空障碍的作用及其是否通过减轻氧化损伤发挥作用。方法:健康成年昆明种小鼠,随机分为对照组、顺铂组、姜黄素组和顺铂+姜黄素灌胃1天、5天、10天、15天、20天和30天组,每组8只。用药结束后24小时测量胃残留率并取胃组织检测MDA和SOD含量。结果:注射顺铂后,各组小鼠体重明显减轻,姜黄素灌胃10~30天可明显减轻顺铂导致的体重减少(P0.05);注射顺铂后各组胃残留率升高(P0.05),而姜黄素预先灌胃10~30天可明显减轻顺铂导致的胃残留率增高(P0.05),各组间治疗效应无明显差异。姜黄素灌胃1~5天组小鼠体重和胃残留率都无显著改善。各组胃组织中MDA和SOD含量差异无统计学意义(P0.05)。结论:姜黄素预先灌胃10天以上可改善顺铂所致的小鼠胃排空障碍,但延长天数并不会有进一步改善;其作用可能不主要通过抗氧化途径。     

Ets-1在姜黄素抑制心脏纤维化的表达研究

目的:研究姜黄素的抗增殖作用是否依赖于其对Ets-1表达的下调。方法:使用Ets-1 siRNA对CFs细胞Ets-1基因进行沉默;Real-time PCR和western-blot法测定各组细胞Ets-1 mRNA和蛋白的表达水平。结果:在mRNA和蛋白水平上,AngⅡ明显增加CFs细胞内Ets-1的表达;使用siRNA技术对Ets-1进行沉默后,随着Ets-1表达的降低及转录调节能力的下降,由AngⅡ诱导的CFs细胞的增殖能力及增殖相关细胞因子分泌减少;姜黄素可以显著降低AngⅡ诱导的Ets-1表达升高,并具有浓度依赖性(P0.05)。说明姜黄素对AngⅡ诱导的CFs增殖的抑制作用可能依赖于其对Ets-1表达的抑制作用。结论:Ets-1 siRNA对Ets-1进行基因沉默后,显示出抗增殖效用;姜黄素能够有效地抑制AngⅡ诱导的CFs细胞Ets-1 mRNA和蛋白的过表达;姜黄素的抗增殖作用可能依赖于其对Ets-1基因的表达下调而得以实现的。     

Ameliorative effects of resveratrol on liver injury in streptozotocin‐induced diabetic rats

The objective of this study was to investigate the ameliorative property and potential mechanism of resveratrol (RVT) in a dose of 10 mg/kg for 15 consecutive days against liver injury in streptozotocin‐induced diabetic rats. Diabetic rats significantly (P < 0.05) exhibited liver injury manifested by increased aspartylaminotransferase, alanine aminotransferase, and bilirubin; disturbed liver weight to body weight; and confirmed by hematoxylin and eosin staining. Liver from diabetic rats exhibited significant increase in malondialdehyde level and significant decrease in reduced glutathione, glutathione‐S‐transferase, quinone reductase, catalase, and superoxide dismutase. Diabetic rats showed significant disturbance in serum lipid profile. Treatment with RVT significantly (P < 0.05) abrogated diabetes‐induced perturbation in these parameters and liver histology. These data suggest that RVT treatment is associated with promising hepatoprotective effect against diabetes‐induced liver damage via reduction of serum glucose level and oxidative damage and improving serum lipid profile. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:384–392, 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21432     

Neuro‐Modulation of Immuno‐Endocrine Response Induced by Kaliotoxin of Androctonus Scorpion Venom

Kaliotoxin (KTX), a specific blocker of potassium channels, exerts various toxic effects due to its action on the central nervous system. Its use in experimental model could help the understanding of the cellular and molecular mechanisms involved in the neuropathological processes related to potassium channel dysfunctions. In this study, the ability of KTX to stimulate neuro‐immuno‐endocrine axis was investigated. As results, the intracerebroventricular injection of KTX leads to severe structural–functional alterations of both hypothalamus and thyroid. These alterations were characterized by a massive release of hormones’ markers of thyroid function associated with damaged tissue which was infiltrated by inflammatory cell and an imbalanced redox status. Taken together, these data highlight that KTX is able to modulate the neuro‐endocrine response after binding to its targets leading to the hypothalamus and the thyroid stimulation, probably by inflammatory response activation and the installation of oxidative stress in these organs.     

Angiotensin‐Converting Enzyme Inhibition and Angiotensin AT1 Receptor Blockade Downregulate Angiotensin‐Converting Enzyme Expression and Attenuate Renal Injury in Streptozotocin‐Induced Diabetic Rats

Angiotensin‐converting enzyme (ACE) is upregulated in the diabetic kidney and contributes to renal injury. This study investigates the possible beneficial effects of the ACE inhibitor (ACEI), enalapril and the AT1 receptor blocker (ARB), valsartan, on renal ACE expression, renal structure, and function in streptozotocin (STZ)‐induced diabetic rats. Male Wistar rats were allocated into four groups: control, STZ‐diabetic rats, and STZ‐diabetic rats treated with either enalapril (10 mg/kg/day) or valsartan (50 mg/kg/day) for 8 weeks. Enalapril and valsartan reduced renal ACE mRNA and protein expression, Na⁺/K⁺‐ATPase activity, oxidative stress, and serum transforming growth factor‐β1 levels compared to the diabetic group. Both treatments normalized renal nitrate/nitrite levels and ameliorated the observed histopathological changes. In conclusion, ACE downregulation by ACEI and ARB indicates that angiotensin II upregulates ACE through AT1 receptor. Prevention of diabetes‐induced changes in ACE expression and Na⁺/K⁺‐ATPase activity could be a new explanation of the renoprotective effects of ACEIs and ARBs. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:378‐387, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21500     

姜黄素灌胃对糖尿病大鼠心肌酶和氧化指标的影响

目的:探讨姜黄素灌胃对糖尿病心脏病变大鼠心肌酶和氧化指标的影响。方法:将成年雄性SD大鼠随机分为对照组、糖尿病组、姜黄素治疗2周组与姜黄素治疗4周组。取心室肌组织匀浆分别检测心肌酶、超氧化物歧化酶(Superoxide dismutase,SOD)和丙二醛(Malondialdehyde,MDA)的含量。结果:糖尿病组与对照组比较,心肌酶天冬氨酸氨基转移酶(Aspartate transaminase,AST)、乳酸脱氢酶(Lactic dehydrogenase,LDH)、肌酸激酶(Creatinekinase,CK)、肌酸激酶同工酶(Creatine kinase isoenzyme-MB,CK-MB)均增高(P0.01)。心肌氧化代谢产物MDA含量升高(P0.01),抗氧化损伤的SOD含量降低(P0.01);姜黄素治疗组与糖尿病组相比,各心肌酶含量有所下降,治疗4周组有明显统计学差异(P0.01)。同时心肌SOD和MDA含量在治疗组均有显著改善(P0.05或P0.01),治疗4周组心肌组织SOD含量较2周组明显升高(P0.05)。结论:姜黄素灌胃可以减轻糖尿病大鼠心肌损伤,提高抗氧化能力。     

Influence of treatment of diabetic rats with combinations of pycnogenol, β‐carotene,and α‐lipoic acid on parameters of oxidative stress

Treatment with antioxidants may act more effectively to alter markers of free radical damage in combinations than singly. This study has determined whether treatment with combinations of pycnogenol, β‐carotene, and α‐lipoic acid was more effective at reducing oxidative stress in diabetic rats than treatment with these antioxidants alone. It is not feasible, based on this study, to assume that there are interactive effects that make combinations of these antioxidants more effective than any one alone to combat oxidative stress. Female Sprague‐Dawley rats, normal and streptozotocin‐induced diabetic, were treated (10 mg/kg/day ip for 14 days) with pycnogenol, β‐carotene, pycnogenol + β‐carotene, or pycnogenol + β‐carotene + α‐lipoic acid; controls were untreated. Concentrations of thiobarbituric acid reactive substances, glutathione and glutathione disulfide, and activities of glutathione reductase, glutathione peroxidase, superoxide dismutase, and catalase were measured in liver, kidney, and heart. Four types of effects were observed: (1) treatment with β‐carotene alone either reversed (cardiac glutathione disulfide) or elevated (cardiac glutathione, hepatic glutathione peroxidase activity) levels seen in diabetic animals; (2) β‐carotene alone produced no effect, but pycnogenol both alone and in combinations elevated (renal glutathione peroxidase and glutathione reductase activities, hepatic glutathione reductase activity and glutathione disulfide) or depressed (cardiac glutathione disulfide) levels seen in untreated diabetic animals; (3) all treatments with antioxidants, either alone or in combination, either normalized (lipid peroxidation in all tissues), elevated (hepatic GSH, cardiac glutathione peroxidase activity), or had no effect on (activities of hepatic catalase and superoxide dismutase in all tissues) levels seen in diabetic animals; (4) in only one case (cardiac glutathione reductase activity) levels in diabetic animals treated with combinations of antioxidants were normal, but elevated in animals treated with either antioxidant alone. Antioxidant effects seem to be dependent on the nature of the antioxidant used and not on combination effects. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:345–352, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20046     

Anti-ischemic Effect of Curcumin in Rat Brain

Turmeric has been in use since ancient times as a condiment and due to its medicinal properties. Curcumin, the yellow colouring principle in turmeric, is polyphenolic and major active constituent. Besides anti-inflammatory, thrombolytic and anticarcinogenic activities, curcumin also possesses strong antioxidant property. In view of the novel combination of properties, neuroprotective efficacy of curcumin was studied in rat middle cerebral artery occlusion (MCAO) model. Rats were subjected to 2 h of focal ischemia followed by 72 h of reperfusion. They were pre-treated with curcumin (100 mg/kg, po) for 5 days prior to MCAO and for another 3 days after MCAO. The parameters studied were behavioural, biochemical and histological. Treatment with curcumin could significantly improve neurobehavioral performance compared to untreated ischemic rats as judged by its effect on rota-rod performance and grid walking. A significant inhibition in lipid peroxidation and an increase in superoxide dismutase (SOD) activity in corpus striatum and cerebral cortex was observed following treatment with curcumin in MCAO rats as compared to MCAO group. Intracellular calcium levels were decreased following treatment with curcumin in MCAO rats. Histologically, a reduction in the infarct area from 33% to 24% was observed in MCAO rats treated with curcumin. The study demonstrates the protective efficacy of curcumin in rat MCAO model.     

Morin Hydrate Mitigates Cisplatin‐Induced Renal and Hepatic Injury by Impeding Oxidative/Nitrosative Stress and Inflammation in Mice

Cisplatin is a widely used chemotherapeutic drug; however, it induces damage on kidney and liver at clinically effective higher doses. Morin hydrate possesses antioxidant, anti‐inflammatory, and anticancer properties. Therefore, we aimed to investigate the effects of morin hydrate (50 and 100 mg/kg, orally) against the renohepatic toxicity induced by a high dose of cisplatin (20 mg/kg, intraperitoneally). Renal and hepatic function, oxidative/nitrosative stress, and inflammatory markers along with histopathology were evaluated. Morin hydrate ameliorated cisplatin‐induced renohepatic toxicity significantly at 100 mg/kg as evidenced from the significant reversal of cisplatin‐induced body weight loss, mortality, functional and structural alterations of kidney, and liver. The protective role offered by morin hydrate against cisplatin‐induced renohepatic toxicity is by virtue of its free radical scavenging property, thereby abating the depletion of cellular antioxidant defense components and through modulation of inflammatory cytokines. We speculate morin hydrate as a protective candidate against renohepatic toxicity of cisplatin.