芝麻素对大鼠化学性心肌损伤的保护作用(1)
摘要：目的 探討芝麻素(Ses)对大鼠化学性心肌损伤的保护作用及可能机制。方法 SD大鼠30只，随机分为正常组、模型组和Ses组，每组10只。模型组和Ses组SD大鼠给予D-半乳糖[180 mg·(kg·d)，i.p.]和三氯化铝[15 mg/(kg·d)，i.g.]造模12周，Ses组于第13周给予Ses[160 mg/(kg·d)，i.g.]治疗，连续8周，正常组给予生理盐水[5.0 ml/(kg·d)，i.g.]。末次给药后称体重(BW)和全心湿重(HWW);HE染色观察心肌病理组织学变化;免疫组化检测心肌iNOS蛋白表达。结果 模型组HWW和HWI高于正常组(P<0.01)，Ses组HWW和HWI均低于模型组(P<0.05);光镜下观察，正常组大鼠心肌细胞间隙、组织形态正常，呈长梭形，心肌纤维结构清晰整齐。模型组心肌细胞增生肥大，心肌纤维增粗且排列紊乱，细胞核增大。与模型组相比，Ses组心肌细胞增生均有不同程度的改善，心肌纤维排列较为整齐，细胞间隙小于模型组;免疫组化图像显示iNOS蛋白主要表达于心肌细胞胞浆中。与正常组相比，模型组iNOS蛋白明显升高(P<0.01);与模型组相比，Ses组心肌iNOS蛋白表达降低(P<0.01)。结论 Ses能下调iNOS蛋白表达，减少NO产生，提高抗氧化能力，发挥保护心肌损伤的作用。
, http://www.100md.com
关键词：芝麻素;心肌;iNOS;化学性心肌损伤
中图分类号：R285.5 文献标识码：A DOI：10.3969/j.issn.1006-1959.2019.08.001
文章编号：1006-1959(2019)08-0001-03
Abstract：Objective To investigate the protective effect and possible mechanism of sesamin (Ses) on chemical myocardial injury in rats. Methods 30 SD rats were randomly divided into normal group， model group and Ses group， with 10 rats in each group. Two groups of SD rats were given D-galactose [180 mg·(kg·d)，i.p.] and aluminum trichloride [15 mg/(kg·d)，i.g.] for 12 weeks. The Ses group was treated with Ses [160 mg/(kg·d)，i.g.] at the 13th week for 8 weeks and the normal group [5.0 ml/(kg·d)，i.g.]. Body weight (BW) and whole heart wet weight (HWW) were measured after the last administration; myocardial histopathological changes were observed by HE staining; myocardial iNOS protein expression was detected by immunohistochemistry. Results HWW and HWI in the model group were higher than those in the normal group (P<0.01). The HWW and HWI in the Ses group were lower than those in the model group (P<0.05). Under the light microscope， the myocardial cell gap and tissue morphology in the normal group were normal. Long fusiform， myocardial fiber structure is clear and tidy. In the model group， the cardiomyocytes proliferated and hypertrophied， the myocardial fibers were thickened and arranged disorderly， and the nucleus increased. Compared with the model group， the myocardial cell proliferation in the Ses group was improved to some extent. The myocardial fibers were arranged neatly and the cell gap was smaller than that in the model group. Immunohistochemical images showed that iNOS protein was mainly expressed in the cytoplasm of cardiomyocytes. Compared with the normal group， the iNOS protein in the model group was significantly increased (P<0.01). Compared with the model group， the expression of iNOS protein in the Ses group was decreased (P<0.01). Conclusion Ses can down-regulate the expression of iNOS protein， reduce the production of NO， increase the antioxidant capacity， and play a role in protecting myocardial injury., 百拇医药(李伟 王欢 姚海 杨解人)
, http://www.100md.com
关键词：芝麻素;心肌;iNOS;化学性心肌损伤
中图分类号：R285.5 文献标识码：A DOI：10.3969/j.issn.1006-1959.2019.08.001
文章编号：1006-1959(2019)08-0001-03
Abstract：Objective To investigate the protective effect and possible mechanism of sesamin (Ses) on chemical myocardial injury in rats. Methods 30 SD rats were randomly divided into normal group， model group and Ses group， with 10 rats in each group. Two groups of SD rats were given D-galactose [180 mg·(kg·d)，i.p.] and aluminum trichloride [15 mg/(kg·d)，i.g.] for 12 weeks. The Ses group was treated with Ses [160 mg/(kg·d)，i.g.] at the 13th week for 8 weeks and the normal group [5.0 ml/(kg·d)，i.g.]. Body weight (BW) and whole heart wet weight (HWW) were measured after the last administration; myocardial histopathological changes were observed by HE staining; myocardial iNOS protein expression was detected by immunohistochemistry. Results HWW and HWI in the model group were higher than those in the normal group (P<0.01). The HWW and HWI in the Ses group were lower than those in the model group (P<0.05). Under the light microscope， the myocardial cell gap and tissue morphology in the normal group were normal. Long fusiform， myocardial fiber structure is clear and tidy. In the model group， the cardiomyocytes proliferated and hypertrophied， the myocardial fibers were thickened and arranged disorderly， and the nucleus increased. Compared with the model group， the myocardial cell proliferation in the Ses group was improved to some extent. The myocardial fibers were arranged neatly and the cell gap was smaller than that in the model group. Immunohistochemical images showed that iNOS protein was mainly expressed in the cytoplasm of cardiomyocytes. Compared with the normal group， the iNOS protein in the model group was significantly increased (P<0.01). Compared with the model group， the expression of iNOS protein in the Ses group was decreased (P<0.01). Conclusion Ses can down-regulate the expression of iNOS protein， reduce the production of NO， increase the antioxidant capacity， and play a role in protecting myocardial injury., 百拇医药(李伟 王欢 姚海 杨解人)