| 引用本文: | 孙赛格,周星宇,宋梓毓,付丹,钱凯.大黄素调控炎症和氧化应激改善小鼠心肌肥厚的研究[J].中国现代应用药学,2025,42(8):7-14. |
| sunsaige,zhouxingyu,songziyu,fudan,qiankai.Emodin Improves Myocardial Remodeling By Anti-inflammatory And Antioxidant Atress[J].Chin J Mod Appl Pharm(中国现代应用药学),2025,42(8):7-14. |
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| 摘要: |
| 目的：通过腹腔注射异丙肾上腺素构建小鼠心肌肥厚模型，观察大黄素改善心肌肥厚的药理作用，并初步探讨大黄素的作用机制。方法：将40只SPF级小鼠随机分成4组，每组10只，分别为空白组、大黄素组、模型组、大黄素给药组。模型组小鼠连续4周每日腹腔注射ISO，给药剂量5mg/kg。大黄素组每日灌胃给药50mg/kg，连续14天。给药结束后，观察各组心重比及心脏形态，HE染色观察心脏组织病理变化，利用试剂盒检测血清中GSH及MDA含量。Western blot分析大黄素抗纤维化、抗炎、抗氧化作用。结果：与对照组相比，模型组小鼠心重比、血清MDA含量、ANP、BNP、β-MHC、Collagen I、TGF-β、TNF-α、IL-6蛋白表达水平显著升高，血清GSH含量、SOD、CAT蛋白表达水平显著下降，大黄素给药后，小鼠心重比显著降低，上述炎症及氧化应激相关指标均有所改善。结论：大黄素可有效抑制ISO诱导的小鼠心肌炎症因子表达，调控氧化应激水平，从而改善心肌肥厚。 |
| 关键词: 大黄素 心肌重构 心肌肥厚 药理作用 抗炎 抗氧化 |
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| 基金项目:江西省自然科学基金项目（毕赤酵母制备药物蛋白N端不均一性的研究，20202BABL216078） |
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| Emodin Improves Myocardial Remodeling By Anti-inflammatory And Antioxidant Atress |
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sunsaige, zhouxingyu, songziyu, fudan, qiankai
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Yichun University
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| Abstract: |
| OBJECTIVE To establish a mouse model of myocardial hypertrophy by intrabitoneal injection of isoproterenol, observe the pharmacological effect of emodin on improving myocardial hypertrophy, and explore the mechanism of emodin. METHODS 40 SPF mice were randomly divided into 4 groups with 10 mice in each group, which were blank group, emodin group, model group and emodin administration group. Mice in the model group were intraperitoneally injected with ISO daily for 4 weeks at a dose of 5mg/kg. Emodin group was given 50mg/kg intragastric daily for 14 days. After administration, the heart weight ratio and cardiac morphology of each group were observed, the pathological changes of heart tissue were observed by HE staining, and the serum GSH and MDA contents were detected by kit. Western blot analysis of emodin's antifibrotic, anti-inflammatory and antioxidant effects. RESULTS Compared with the control group, the heart-to-weight ratio, serum MDA content, ANP, BNP, β-MHC, Collagen I, TGF-β, TNF-α and IL-6 protein expression levels of the model group were significantly increased, while the serum GSH content, SOD and CAT protein expression levels were significantly decreased. After emodin administration, the heart-to-weight ratio of mice was significantly decreased. The above inflammatory and oxidative stress related indexes were improved. CONCLUSION Emodin can effectively inhibit the expression of ISO-induced myocardial inflammatory factors in mice, regulate the level of oxidative stress, and improve myocardial hypertrophy. |
| Key words: Emodin Myocardial remodeling Myocardial hypertrophy Pharmacological action |
