Background: Lead (Pb) disturbs of oxidant/antioxidant balance in testicular cells causing oxidative stress. Crocin (Cr) and pumpkin seed oil (PSO) have antioxidant effects and neutralize free radicals. Aim: This study was performed to assess the cytotoxicity of lead on testis and the possible protective effect of Cr and PSO. Methods: Forty eight healthy male rats were divided into six groups as follows: Control group, Cr group: each rat was received Crocin (200 mg/kg) given intraperitonealy (ip) once daily for 4 weeks, PSO group: each rat was orally received PSO (1 ml/kg) daily for 4 weeks , Pb group: each rat was received lead acetate, (8 mg/kg) ip daily for 4 weeks, (Cr+ Pb) group: each rat was received (200 mg/kg) crocin ip with 8 mg/kg Pb ip for 4 weeks and (PSO+ Pb) group: each rat was received PSO (1 ml/kg) orally in addition to ip lead acetate (8 mg/kg) daily for 4 weeks. The testicular tissues have been processed for a light microscopic study. Results: In Pb -treated rats, levels of FSH, LH, and testosterone significantly decreased. Decrease thickness of spermatogenic layers, mispresentation, Vacuolations, degeneration of spermatogenic cells, wide interstitial spaces, Weak PCNA and androgen receptor immunoexpression were observed. Both Cr and PSO treatment resulted in reversing Pb effects on testis presented in improvement in hormonal levels and histological architecture of most of seminiferous tubules with increase PCNA and androgen receptor immunoexpressions. Conclusions: Cr and PSO may have ameliorative effects after lead acetate toxicity on rat testis.
Background: Hepatic fibrosis is an important medical disease with high rates of morbidity and mortality. Bone marrow mesenchymal stem cells have been recommended as a powerful therapy for treatment of liver fibrosis. Simvastatin has an ameliorative effect on fibrosis of different organs.The study aimed at comparing between the effect of BM-MSCs and simvastatin in treatment of liver fibrosis induced by carbon tetrachloride. Material and Methods: Fifty rats were categorized into, group I control group, group II in which rats injected by CCl4 to induce hepatic fibrosis. Group III in which rats were injected by CCL4,then injected intravenously by a single dose of BM-MSCs, group IV in which rats were injected by CCL4 then given simvastatin orally once daily for eight weeks. Group V in which rats were given both BM-MSC and simvastatin. At the end of the experimental study, blood samples were collected for biochemical analysis and liver tissues were prepared for histological and immunohistochemical examination. Results: CCL4 significantly elevated liver enzymes and induced destruction of normal hepatic structures with significant elevation of mean area percentage of collagen fibers deposition and TGF- expression. BM-MSC and simvastatin improved liver enzymes and histological structure of liver tissue, but the anti-fibrotic effect of BM-MSC was superior to that of simvastatin. Moreover, combination of BM-MSC and simvastatin exerted strong anti-fibrotic effect and preserved normal histologic structure of liver tissue more than each of them alone. Conclusion: A combination of BM-MSCs and simvastatin has an ameliorative role in the treatment of liver fibrosis induced by CCl4.
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