Pretreatment with berberine protects against cisplatin-induced renal injury in male Wistar rats.

Berberine (BBR), an isoquinoline alkaloid, has been reported to be an antioxidant agent. This study was conducted to investigate the effect of BBR against nephrotoxicity induced by cisplatin (Cis) in male rats. In this experimental study, 28 Wistar male rats were randomly divided into four groups. Rats were pretreated with BBR (100 mg/kg/day, p.o.) for 7 consecutive days and Cis (7.5 mg/kg, i.p.) was administrated on the 7th day, 1 h after the last dose of BBR. Blood samples were collected to determine blood urea nitrogen (BUN) and creatinine (Cr) levels. Malondialdehyde (MDA), glutathione (GSH), protein carbonyl (PC), and nitric oxide (NO) levels and the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and myeloperoxidase (MPO) were assessed in the left renal tissue. Also, the mRNA expression of SOD2 and PGx1 was measured in the left renal tissue. The right kidney was used for histopathological evaluation. Our results revealed that the levels of Cr, BUN, MDA, NO, and PC and the MPO activity increased by Cis administration. Also, we found that Cis decreased renal GSH level and SOD, GPx, and CAT activities. Pretreatment with BBR for 7 consecutive days significantly attenuated the Cis-induced nephrotoxicity via increasing the antioxidant capacity and reducing the oxidative stress indices in the renal tissue. Moreover, the renoprotective effect of BBR was confirmed by the histopathological evaluation of the kidneys. Our results indicated that BBR has produced amelioration in biochemical indices and oxidative stress parameters against Cis-induced nephrotoxicity.

Ellagic acid as a potential antioxidant, alleviates methotrexate-induced hepatotoxicity in male rats.

BACKGROUND: Hepatotoxicity is one of the most life-threatening side-effects of Methotrexate therapy. Former studies highlighted the significance of oxidative stress in promoting Methotrexate-induced hepatotoxicity (MIH). Hence, the current study investigated the protective effect of Ellagic acid (EA), a poly-phenolic antioxidant, against MIH. METHODS: Twenty-eight male Wistar rats were grouped into four sets: group 1 (control), group 2 (injected intraperitoneally with 20 mg/kg of Methotrexate on the 9th day), group 3 (treated orally with 10 mg/kg/day of EA for 10 days and injected with Methotrexate on the 9th day) and group 4 (treated with EA for 10 days). Subsequently, biochemical and histopathological parameters were evaluated in serum samples and liver tissues. RESULTS: Methotrexate significantly increased activities of aminotransferases and ALP enzymes as well as levels of oxidative stress parameters in liver tissue. Likewise, Methotrexate decreased hepatic reduced glutathione level and activities of antioxidant enzymes. EA pre-treatment markedly attenuated the activities of aminotransferases and ALP, levels of oxidative stress parameters and augmented activities of antioxidant enzymes. Similarly, the remarkable protective effect of EA on liver has been confirmed by histological examination. CONCLUSION: In sum, the current study supports the hypothesis that EA may be used as a promising pre-therapy to prevent the MIH.

Ellagic acid mitigates sodium arsenite-induced renal and hepatic toxicity in male Wistar rats.

BACKGROUND: The aim of this study was to investigate the effect of ellagic acid (EA) on arsenic-induced renal and hepatic toxicity in rats. METHODS: A total number of 35 male Wistar rats were randomly divided into five experimental groups. Group 1 received normal saline (po). Group 2 received sodium arsenite (SA, 10mg/kg, po) for 21days. Group 3 received EA (30mg/kg, po) for 14days. Groups 4 and 5 received SA 7days prior to EA (10 and 30mg/kg respectively) treatment and continued up to 21days simultaneous with SA administration. Various biochemical, histological and molecular biomarkers were measured in kidney and liver. RESULTS: Treatment with EA (more potently at dose of 30mg/kg) restored the SA-induced alterations in serum creatinine (Cr) and blood urine nitrogen (BUN) levels as well as the changes in aspartate aminotransferase (AST), alkaline phosphatase (ALP) and alanine aminotransferase (ALT) concentrations (all p<0.001). Elevated levels of malondialdehyde (MDA) and nitric oxide (NO) in renal and hepatic tissue was reduced by EA treatment (all p<0.001). Treatment with EA enhanced the glutathione (GSH) content in liver (p<0.001) and up-regulated renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) mRNA expression (all p<0.001). The SA-induced histopathological alterations in kidney and liver were reduced by EA treatment. CONCLUSION: In conclusion, the presence of EA with SA alleviated its toxic effects and EA treatment might be an effective strategy for the management of arsenic-induced renal and hepatic damage.

Effects of herbal extracts and compounds and pharmacological agents on pulmonary fibrosis in animal models: a review.

Pulmonary fibrosis, a chronic inflammatory disease that occurs mainly in older adults, is a serious health threat with few effective treatment options. The etiological aspects of pulmonary fibrosis remain unknown, though some factors such as cigarette smoking, viral infections, surfactant protein polymorphisms, and chronic or high doses use of certain drugs are considered to be risk factors for the progression of pulmonary fibrosis. No standard treatments have been introduced in clinic yet. Although glucocorticoids and antioxidant drugs have been administered, the severe and broad-spectrum adverse effects of glucocorticoids limit their use. Efforts to identify novel therapeutic agents with improved safety profiles are therefore ongoing. In this review, the authors have described the effects of herbal extracts and compounds and certain pharmacological agents on pulmonary fibrosis in animal models. These effects indicate that herbs are a promising source of compounds that can play pivotal roles in the treatment of lung fibrosis.