Protective Effects of Zingerone on Oxidative Stress in Doxorubicin-Induced Rat Hepatotoxicity.

Montelukast, a leukotriene receptor antagonist abrogates lipopolysaccharide-induced toxicity and oxidative stress in rat liver

Background: Methotrexate as a chemotherapy agent causes oxidative stress in the liver. Chicory (Cichorium intybus), a member of the Asteraceae family, is a well-known herb possessing various biological activities. Objectives: The present study was conducted to assess the protective effect of Cichorium intybus extract against methotrexate-induced oxidative stress in rats. Methods: Thirty male Wistar rats were divided into five groups. The negative control group was administered 5 mL/kg of normal saline. In the positive control group, normal saline was administered for 11 days, and a single dose of methotrexate (MTX; 20 mg/kg, i.p) was injected on the 7th day. Groups 3 - 5 received Cichorium intybus extract (CIE) at the doses of 100, 200, and 400 mg/kg p.o., respectively, for 11 days, and a single dose of MTX was administered on the 7th day. The animals were sacrificed 24 h after the last injection. Blood samples were withdrawn to measure serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB) levels. Glutathione (GSH), malondialdehyde (MDA) levels and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were assayed in liver tissues. A portion of the liver tissues was used for histological examination. Results: The results showed a dramatic reduction in the levels of AST, ALT, ALP, GSH, CAT, SOD, and GPx and a significant increase in the levels of TB and MDA by MTX administration. The groups pretreated with CIE showed a significant increase in the levels of AST, ALT, ALP, GSH, CAT, SOD, and GPx and a significant decrease in the levels of TB and MDA at all the doses, but the most significant change was observed at the dose of 400 mg/kg (P < 0.05). Our histological findings confirmed the above-mentioned results. Conclusions: The results revealed that Cichorium intybus has protective effects against the liver tissue damage induced by MTX.

Cisplatin has potent antitumor properties. It has several toxic side effects, such as hepatotoxicity. It is thought that hepatotoxicity induced by cisplatin is caused by oxidative stress. It has shown that calcium dobesilate (CD) has potent antioxidant properties. The present study aimed to assess CD protective effects on cisplatin-induced hepatotoxicity in mice. In this study, 28 mice were selected randomly and were divided into four groups, including control, cisplatin (20 mg/kg, i.p., only on the first day of the experiment), Cisplatin+CD 50 (50 mg/kg CD, orally), and Cisplatin+CD 100 (cisplatin with 100 mg/kg CD, orally). A 4-day oral gavage of CD was applied to the treated groups. The mice were sacrificed on the 5th day, and serum glutamic pyruvic transaminase (SGPT), serum glutamic-oxaloacetic transaminase (SGOT), alkaline phosphatase (ALP), malondialdehyde (MDA) and reactive oxygen species (ROS) levels, superoxide dismutase (SOD), and glutathione peroxidase (GPx) enzyme activity levels in liver tissue were evaluated. Histopathological evaluation was assessed using hematoxylin and eosin-stained liver tissue sections. The results indicated that there was a significant increase in GSPT, SGOT, ALP, and MDA and also a significant reduction in the liver activity of SOD and GPx in cisplatin-treated animals. Treatment with CD (100 mg/kg) remarkably attenuated the GSPT, SGOT, ALP, MDA, and ROS levels. Moreover, CD (100 mg/kg) elevated the SOD and GPx activity in the liver tissue of cisplatin-treated mice. The findings showed that CD has a protective effect against cisplatin-induced hepatotoxicity, at least by improving the antioxidant parameters.

To study the effect of glucagon-likepeptide 1(GLP-1)receptor agonist on insulin resistance and hepatic oxidative stress in rats with diabetes mellitus combined with nonalcoholic fatty liver disease. 36 male SD rats were served as the experimental animal and randomly divided into control group, model group, and GLP-1 group. The rats of control group were given routine diet with intraperitoneal injection of normal saline, those in model group were given high fat diet and intraperitoneal injection of normal saline, while GLP-1 group rats were fed with high fat diet and intraperitoneal injection of liraglutide. After 4 weeks of treatment, insulin resistance, lipid metabolism, liver injury and oxidative stress were all assessed. Serum fasting blood glucose, fasting insulin, total cholesterol, triglyceride, alanine transaminase(ALT), aspartate transaminase(AST)levels and total cholesterol, triglyceride contents in liver tissue, and as well as homeostasis model assessment for insulin resistance(HOMA-IR)levels of model group were significantly higher than those of control group, complex insulin sensitivity index(ISIcomp)level was significantly lower than that of control group; serum fasting blood glucose, fasting insulin, total cholesterol, triglyceride, ALT, AST contents and HOMA-IR levels of GLP-1 group were significantly lower than those of model group, ISIcomp level was significantly higher than that of model group; superoxide dismutase(SOD), glutathione peroxidase(GSH-Px), catalase(CAT)contents in liver tissue of model group were significantly lower, while malondialdehyde content and SOD, GSH-Px, CAT, NF-E2 related factor-2(Nrf-2), antioxidant response element(ARE), heme oxygenase-1(HO-1), quinone oxidoreductase-1(NQO-1), glutathione thiol transferase(GST)mRNA expression were significantly higher than control group; SOD, GSH-Px, CAT contents and SOD, GSH-Px, CAT, Nrf-2, ARE, HO-1, NQO-1, GST mRNA expression in the liver tissue of GLP-1 group were significantly higher, while malondialdehyde content was significantly lower than that of model group. GLP-1 receptor agonist reduces insulin resistance and liver oxidative stress injury in diabetic rats with nonalcoholic liver disease. (Chin J Endocrinol Metab, 2017, 33: 228-232) Key words: Diabetes mellitus, type 2; Nonalcoholic fatty liver disease; Glucagon like peptide -1; Insulin resistance; Oxidative stress

Doxorubicin (DOX), a potent broad‑spectrum chemotherapeutic agent used for the treatment of several types of cancer, is largely limited due to its serious side effects on non‑target organs. Thus, the present study aimed to investigate whether berberine (Ber), an isoquinoline alkaloid, could reduce DOX‑induced acute hepatorenal toxicity in rats. Fifty rats were randomly divided into five groups: i)Control group, ii)DOX group, iii)DOX+Ber (5mg kg) group; iv)DOX+Ber (10mg kg), and v)DOX+Ber (20mg kg) group. In the tests, body weight, organ index, general condition and mortality were observed. In addition, the serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), total cholesterol (TCHO) and blood urea nitrogen (BUN) were determined to evaluate hepatorenal function. Hepatorenal toxicity was further assessed using hematoxylin and eosin stained sections. Furthermore, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdehyde (MDA) in rat serum or tissue homogenate were also assessed to determine the mechanisms of action. Results suggested that pretreatment with Ber ameliorated the DOX‑induced liver and kidney injury by lowering the serum ALT, AST, TCHO and BUN levels, and the damage observed histologically, such as hemorrhage and focal necrosis of liver and kidney tissues induced by DOX were also attenuated by Ber. Furthermore, Ber also exerted certain antioxidative properties through reversing the changes in the levels of MDA, SOD, GSH and MDA induced by DOX. These findings indicate that Ber has protective effects against DOX‑induced acute hepatorenal toxicity in rats. Combination of Ber with DOX is a novel strategy that has the potential for protecting against DOX‑induced hepatorenal toxicity in clinical practice.

Effect of Ginkgo biloba on liver injury of arsenic poisoning rats caused by corn flour baked by high-arsenic coal

Objective To investigate the effect and mechanism of irisin postconditioning on hepatic ischemia reperfusion injury in rats. Methods Totally 36 SD rats were randomly divided into sham group (S), model group (I/R) and irisin group (Ir), with 12 rats in each group. Hepatic ischemia was constructed in model group and irisin group by ligating left middle lobe of liver vascular branches for 60 min. Irisin was administered at the beginning of reperfusion by intravenous injection at the concentration of 10 μg/kg for rats in irisin group. We only dissected the hepatic duodenal ligament of rats in the S group. Serum and liver tissues were collected at 6 h after reperfusion through the inferior chamber. The serum levels of alanine aminotransferase (ALT), glutamic oxalacetic transaminase (AST), interleukin (IL)-6, IL-1βand tumor necrosis factor-α (TNF-α) were examined. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) in liver tissue were measured. The pathological changes of liver tissue were observed by hematoxylin and eosin (HE) staining. The phosphorylations of janus kinase 2 (JAK2), signal transducer and activators of transcription 3 (STAT3) and B cell lymphoma/leukemia-2 (bcl-2), bcl-2 associated X protein (bax), cysteinyl aspartate-specific protease (Caspase)-3 were assessed by Western blotting. Results The ALT levels in S group, I/R group and irisin group were as follows: (75.24±2.65), (705.33±4.02), (385.46±3.58) U/L; The AST levels were as follows: (122.33±6.76), (1 357.54±5.23), (738.26±3.98) U/L; The IL-6 levels were as follows: (104±16), (586±86), (275±35) ng/L; The TNF-α levels were as follows: (92±10), (1 165±102), (511±73) ng/L; The IL-1β levels were as follows: (98±12), (610±79), (312±41) ng/L; The MDA contents were as follows: (174±38), (1 900±460), (1 055±266) ng/L; The SOD contents were as follows: (124±10), (46±8), (70±10) ng/L; The GPX contents were as follows: (106±12), (42±5), (62±11) ng/L; The Caspase-3 levels were as follows: (0.22±0.06), (0.86±0.14), (0.57±0.11) ng/L; The p-JAK2 levels were as follows: 0.44±0.05, 0.91±0.07, 0.62±0.11; The p-STAT3 levels were as follows: 0.35±0.04, 0.86±0.08, 0.57±0.07. As compared with the sham group, the levels of ALT, AST, IL-6, TNF-α, IL-1β, MDA and Caspase-3 were significantly increased (t=445.551, 219.362, 21.700, 7.700, 36.182, 14.132, 24.191, 10.111, 13.753, 7.023, 14.456 and 6.556, P<0.01). The activities of GPX and SOD in model group and irisin group were significantly decreased (t=20.374, 14.104, 15.945 and 10.965, P<0.01), and the pathological damage worsened and the expression levels of activated p-JAK2 and p-STAT3were up-regulated in other groups (t=14.289, 5.479, 19.054 and 8.224, P<0.01); As compared with model group, the levels of ALT, AST, IL-6, TNF-α, IL-1β, MDA and Caspase-3 in irisin group were significantly decreased (t=226.183, 14.000, 14.081, 22.052 and 7.906, P<0.01), and pathological damage was alleviated and the expression levels of activated SOD and GPX significantly increased (t=6.274 and 4.985, P<0.01). The p-JAK2 and p-STAT3 were down-regulated in irisin group (t=8.819 and 10.834, P<0.01). Conclusion Exogenous irisin postconditioning can significantly decrease hepatic ischemia-reperfusion injury in rats by suppressing oxidative stress and cell apoptosis, and the mechanism may be associated with the suppression of JAK2/STAT3 signaling activation. Key words: Irisin; Hepatic ischemia; Reperfusion injury; Janus kinase 2; Signal transducer and activators of transcription 3

Objective The aim of this study is to assess the relationship between T-lymphocyte subsets, regulatory T cells (Treg), and hepatic fibrosis in patients with a nonalcoholic fatty liver disease (NAFLD). Methods A retrospective analysis was conducted on 64 NAFLD patients (research group) and 73 healthy subjects (control group) in our hospital from January 2020 to December 2021. T-lymphocyte subsets (Th17) and Treg, liver function (alanine aminotransferase (ALT), aspartate aminotransferase (AST)), hepatic fibrosis indexes (type III procollagen (PCIII), type IV collagen (CIV), laminin (LN), hyaluronic acid (HA)), inflammatory factors (high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), interleukin-8 (IL-8)), and oxidative stress (OS) response ((superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA)) were tested. The relationship between Th17/Treg and the abovementioned indexes in NAFLD patients was analyzed. Results In comparison to the control group, Th17 and Th17/Treg were higher in the research group (P < 0.05). In addition, liver function, liver fibrosis markers, inflammatory factors, and MDA were elevated, while SOD and GSH-PX decreased (P < 0.05). Subsequently, NAFLD patients were divided into groups A (Th17/Treg <1.15, n = 33) and B (Th17/Treg ≥1.15, n = 31) based on their median Th17/Treg levels. It was seen that liver injury, hepatic fibrosis, inflammation, and OS in group A were more severe (P < 0.05). The Pearson correlation coefficient revealed that Th17/Treg was positively correlated with AST, ALT, PCIII, MDA, and inflammatory factors but negatively correlated with SOD and GSH-PX (P < 0.05).

Doxorubicin (DOX) is one of the most commonly prescribed anti-cancer drugs. However, DOX-induced hepatotoxicity is a dose-limiting side effect. This study aimed to clarify the potential protective effects of metformin on DOX-induced hepatotoxicity in rats. The animals were divided into six groups (n = 6 each): Control Group, DOX group, metformin 200mg/kg group, DOX + metformin 50mg/kg group, DOX + metformin 100mg/kg group, and DOX + metformin 200mg/kg group. Hepatic injury was induced by a single intraperitoneal injection of DOX (20mg/kg). The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) in serum were determined. Furthermore, the hepatic histopathological changes were evaluated. To identify the markers of oxidative stress, the level of malondialdehyde (MDA) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in liver tissue were measured. Results showed that DOX provoked a marked elevation in ALT, AST, and ALP serum levels. In addition, oxidative stress was significantly boosted in DOX-treated rats compared to control rats. All these were abolished with the metformin administration. Histological examination also showed that metformin could substantially reduce DOX-induced alterations. The most prominent effect was observed by high-dose metformin.

Objective To investigate the effect and mechanism of gadolinium chloride alleviates partial warm ischemia-reperfusion injury of liver by suppressing kupffer cell function in mice. Methods Forty-eight male C57BL/6 mice were randomly divided into sham-operated group (Sham), Hepatic ischemia-reperfusion injury (HIRI) group, gdolinium chloride groups (Gd+ IRI), and cobalt protoporphyrin (CoPP+ IRI) group (n=12). The rats were injected with the same dose of normal saline in Sham group and IRI group. Gd+ IRI group were intraperitoneally injected with GdCl3 (20 mg/kg) 24 hours before operation. At the same time, CoPP+ IRI group were intraperitoneally injected with CoPP (5 mg/kg). Except for Sham group, an 70% volume HIRI model was established by means of 60 minutes ischemia and then 6 hours reperfusion in the other groups. The levels of serum aspartate transaminase (AST) and alanine aminotransferase (ALT) in each group were compared. Enzyme-linked immunosorbent assay were used to test the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the liver tissue. The level of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, heme oxygenase-1 (HO-1), and protective factor IL-10 mRNA level were detected by real time quantitative polymerase Chain Reaction (RT-PCR). Immunohistochemical staining was used to measure Fas, FasL protein expression level of extrahepatic biliary epithelial cells. Results Respectively, the serum ALT level in the HIRI, Gd+ IRI and CoPP+ IRI groups was (1 236.7±62.4), (638.9±50.9), (740.3±53.1) U/L, and the AST level was (1 107.8±68.3), (568.5±42.7), (679.1±49.9) U/L, the serum level of ALT and AST in Gd+ IRI and CoPP+ IRI groups was lower than IRI group (t=6.721, P<0.01; t=4.732, P<0.05; t=5.984, P<0.01; t=2.691, P<0.05). Compared with IRI group, the activity of SOD and GSH-Px was promoted (t=7.301, P<0.01; t=1.937, P<0.05), whereas the levels of MDA was reduced (t=9.519, P<0.01; t=8.635, P<0.01). Simultaneously, the TNF-α, IL-1β and IL-6 mRNA level in Gd+ IRI and CoPP+ IRI groups were decreased (t=6.721, P<0.01; t=2.316, P<0.05), and the levels of IL-10 and HO-1 mRNA were increased (t=2.973, P<0.05; t=7.921, P<0.01). After hepatic artery reflow 6 h, the Fas expression levels on bile ducts epithelial cells in Gd+ IRI and CoPP+ IRI groups respectively was 22.4%, 29.7%, which was lower than IRI group (38.9%) (χ2=6.561, P<0.01; χ2=2.547, P<0.05). The FasL expression levels in Gd+ IRI and CoPP+ IRI groups respectively was 21.2%, 25.1%, which was lower than IRI group (36.5%) (χ2=5.982, P<0.05; χ2=3.188, P<0.05). Conclusion Gdolinium chloride shows an protective function aganist liver ischemia-reperfusion iniury in mice by Oxidative stress, inhibiting inflammation and cell apoptosis. The up-regulation of HO-1 by gdolinium chloride may be the possible mechanism. The up-regulation of HO-1 and inhibiting the Fas/FasL protein expression by gdolinium chloride may be the possible mechanism. Key words: Gdolinium chloride; Liver; Ischemia-reperfusion injury; Heme oxygenase-l

Triptolide Alleviates Hepatic Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Inhibiting NF-κB Activity in Mice

Organophosphorous pesticides, commonly used in agriculture for achieving better‐quality products, are toxic substances that have harmful effects on human health. Recent research on pesticides, especially pesticide mixtures, has shown that they are one of the key environmental health issues. The aim of the present study was to investigate the protective effects of Alstonia boonei ethanolic extract in dichlorvos‐induced neurotoxicity in Wistar rats. Dichlorvos (50 mg/kg body weight) was orally administered in Wistar rats for 14 days followed by the treatment of Alstonia boonei (200 and 400 mg/kg body weight) for 14 days. The activities of lipid peroxidation (LPO), reduced glutathione (GSH) and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level were measured to evaluate the toxicity of these pesticides in the brain. Histological examinations of the brain were monitored. Under the influence of dichlorvos, there was significant decrease in the activities of SOD, CAT, GPx, GSH, ALT and AST and significant increase in malondialdehyde. Alstonia boonei showed a significant brain‐protective effect by decreasing the level of lipid peroxidation and elevating the activities of antioxidative enzymes and the level of GSH. Furthermore, histological alterations in the brain were observed in dichlorvos‐untreated rats and were ameliorated in dichlorvos‐induced treated rats with Alstonia boonei. The observations presented lead us to conclude the harmful effects of dichlorovos during the exposure and the protective role of Alstonia boonei in minimizing these effects. Key words: Alstonia boonei, brain, dichlorvos, lipid peroxidation, organophosphate, oxidative stress, reactive oxygen species

Moderating effects of oregano extract (Origanum vulgare L.) on oxidative stress and toxicity induced by organophosphate pesticide, diazinon (0.287 mg/l) were investigated for the first time in rainbow trout, Oncorhynchus mykiss by measuring antioxidant and metabolic enzymes. In non-diazinon-exposed fish, the hepatic levels of total antioxidant capacity (TAC) and antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) elevated in fish supplemented with 6 and 10 g ORG/kg diet compared to control group (non-ORG-supplemented fish). The supplementation of fish with 14 g ORG/kg diet significantly decreased the hepatic antioxidant enzymes compared to control. The acetylcholinesterase (AChE) activity and malondialdehyde (MDA) levels remained unchanged in all groups throughout the experiment. The serum levels of hepatic metabolic enzymes [(aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LHD)] remained unchanged in all experimental groups throughout the experiment. In diazinon-exposed groups, the activity of SOD, GPx, and TAC in liver elevated after exposure to diazinon in fish fed 2, 6, and 10 g ORG/kg diet. The CAT activity increased only in fish supplemented with 6 and 10 g ORG/kg diet. The levels of all antioxidant enzymes and TAC significantly decreased in control and fish supplemented with 14 g ORG/kg diet. The AChE activity significantly declined in control and fish supplemented with 2 and 14 g ORG/kg diet. After exposure to diazinon, the levels of MDA in liver increased in control and those fed 2 and 14 g ORG/kg diet. In fish supplemented with 6 and 10 g ORG/kg diet, the MDA levels showed no significant alternations during the experiment period. The serum levels of AST, ALT, and alkaline phosphatase (ALP) elevated during exposure to diazinon in control and fish supplemented with 2 and 14 g ORG/kg diet, while these enzymes showed no significant changes in fish fed with 6 and 10 g ORG/kg diet. In conclusion, our results showed that ORG at optimum dietary levels (6 and 10 g ORG/kg diet) could moderate the toxicity induced by diazinon in rainbow trout by enhancing the liver antioxidant system and protecting the hepatocytes. Furthermore, the high dietary levels of ORG caused toxic effects on antioxidant enzymes and hepatocytes, which this makes it necessary to optimize its levels in the diet.

A neutrophil elastase inhibitor, sivelestat, attenuates sepsis-induced acute kidney injury by inhibiting oxidative stress

White-skinned sweet potato (WSSP, Ipomoea batatas L.)는 인도네시아 및 다른 나라 등에서 전통약제로 당뇨병 치료에 널리 사용되고 있다. 본 실험에서는 흰 쥐를 streptozotocin (45 mg/kg체중, i.p.)으로 당뇨병을 유발시킨 후 WSSP의 메탄올 추출물을 체중 1 kg당 Dose 100; 200 mg/kg을 경구로 투여하였다. 산화적 스트레스에 대한 보호효과를 평가하였고 그 효능을 인슐린 분비촉진제인 glimepiride (50 mg/kg 체중)와 비교해 보았다. 산화적 스트레스 평가는 WSP 메탄올 추출물과 glimepiride를 2주 투여 한 후 간장조직의 지질 과산화물(LPO)함량, 혈청 AST, ALT, total triglyceride (TG), total cholesterol (TC), 그리고 항산화효소들인 superoxide dismutase (SOD), 카탈라아제(CAT), 글루타치온 과산화물 분해효소(GPx), 글루타치온 S-전이효소(GST)활성도 등을 간장에서 측정하여 시행하였다. 당뇨 흰쥐에서 혈당, LPO 함량, AST, ALT, TG, TC 함량 등은 정상군에 비하여 그 값이 증가하였고, SOD, CAT, GPx, GST 활성도 값은 감소하였다. 당뇨 흰쥐에 WSSP 메탄올 추출물(200 mg/kg)을 2주일 동안 투여한 결과 의미있는 혈당 감소를 볼 수 있었고, LPO, TG, TC, AST, ALT 함량에서도 개선효과를 볼 수 있었다. 또한 SOD, GPx, 그리고 CAT등 항산화효소들의 활성도 증가도 나타났다. 따라서 WSSP 메탄올 추출물은 당뇨쥐의 혈당을 낮추어 산화적 스트레스를 약화시키고 당뇨로 유발된 손상을 보호해 주는 효과가 있다는 결과를 얻었다. Sweet potato (Ipomoea batatas L.) is widely used in Indonesia and other countries as a traditional medicine for the treatment of diabetes mellitus (DM). The MeOH extract of white skinned sweet potatoes (WSSP) was administered orally in doses of 100 and 200 mg/kg body weight in streptozotocin (STZ)-induced diabetic rats. Experimental diabetes was induced by a single dose of STZ (45 mg/kg, i.p.) injection. Oxidative stress was measured by tissue lipid peroxide (LPO) levels, serum aspartate transaminase (AST), alanine transaminase (ALT), total triglyceride (TG), total cholesterol (TC) and by antioxidative enzymatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase in the liver. An increase in blood glucose, LPO level, AST, ALT, TG and TC levels was observed in the STZ-induced diabetic rats. Administration of MeOH extract of WSSP at a dose of 200 mg/kg for two weeks caused a significant reduction in blood glucose, LPO levels, AST, ALT, TG and TC levels in the STZ-induced diabetic rats. Furthermore, oral administration of MeOH extract showed significant improvement in the activities of antioxidant enzymes (SOD, GPx, and CAT) compared to STZ-induced diabetic rats. In conclusion, the obtained results clearly indicate the role of oxidative stress in the induction of diabetes, and that the protective effects of MeOH extracts of WSSP could be used to benefit diabetic patients.