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陶翠宁, 罗春玉, 李忠霄, 钟聪璐, 周婉莹, 卜献春, 谭军, 袁春云.滋膵通脉饮通过调控促炎脂肪因子TNF-α、MCP-1、PAI-1对糖尿病大鼠心肌纤维化的影响[J].湖南中医药大学学报,2026,46(2):240-247[点击复制] |
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| 滋膵通脉饮通过调控促炎脂肪因子TNF-α、MCP-1、PAI-1对糖尿病大鼠心肌纤维化的影响 |
| 陶翠宁,罗春玉,李忠霄,钟聪璐,周婉莹,卜献春,谭军,袁春云 |
| (湖南中医药大学, 湖南 长沙 410208;湖南省中西医结合医院/湖南省中医药研究院附属医院, 湖南 长沙 410006) |
| 摘要: |
| 目的 探讨滋膵通脉饮调控促炎脂肪因子肿瘤坏死因子-α（TNF-α）、单核细胞趋化蛋白-1（MCP-1）、纤溶酶原激活物抑制因子-1（PAI-1）对糖尿病大鼠心肌纤维化的影响。方法 SD大鼠40只，随机选10只作为空白对照组，其余30只采用高糖高脂饮食联合腹腔注射链脲佐菌素（STZ）建立糖尿病心肌病（DCM）模型。将造模成功的大鼠随机分为模型组、滋膵通脉饮组（17.6 g·kg-1）、依那普利组（0.53 mg·kg-1），每组9只。各组给予对应药物灌胃，每天1次，连续6周。治疗前后定期监测各组体质量及空腹血糖（FBG）；采用生化法测定大鼠血清葡萄糖（GLU）、糖化血清蛋白（GSP）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、乳酸脱氢酶（LDH）含量；ELISA检测空腹胰岛素（FINS）水平，并计算胰岛素抵抗指数（HOMA-IR）及胰岛素敏感指数（ISI）；ELISA检测肌酸激酶同工酶（CK-MB）、心肌肌钙蛋白T（cTnT）、Ⅰ型胶原蛋白（COL-Ⅰ）、TNF-α、MCP-1、PAI-1含量。通过HE染色、Masson染色和天狼星红染色观察DCM大鼠心肌组织病理形态学变化，并计算大鼠心肌组织心肌胶原容积分数（CVF）水平。结果 与空白对照组比较，模型组体质量减轻（P<0.01），FBG、GLU、GSP、TC、TG、LDL-C、HOMA-IR、LDH、CK-MB、cTnT、COL-Ⅰ、TNF-α、MCP-1、PAI-1均升高（P<0.01），FINS、ISI降低（P<0.01），大鼠心肌组织结构排列紊乱，心肌纤维间隙增宽伴胶原沉积，心肌细胞出现脂肪变性，存在炎症细胞浸润，CVF升高（P<0.01）。与模型组比较，滋膵通脉饮组体质量增加（P<0.05），FBG、GLU、GSP、TC、TG、LDL-C、HOMA-IR、LDH、CK-MB、cTnT、COL-Ⅰ、TNF-α、MCP-1、PAI-1均降低（P<0.05，P<0.01），FINS、ISI均升高（P<0.05，P<0.01），大鼠心肌纤维排列趋于整齐，心肌细胞形态趋于正常，炎症浸润改善，CVF降低（P<0.01）。结论 滋膵通脉饮可改善DCM大鼠心肌纤维化，其作用机制可能与下调促炎脂肪因子TNF-α、MCP-1、PAI-1的释放，抑制心肌纤维化有关。 |
| 关键词: 糖尿病心肌病 心肌纤维化 滋膵通脉饮 促炎脂肪因子 肿瘤坏死因子-α 单核细胞趋化蛋白-1 纤溶酶原激活物抑制因子-1 |
| DOI：10.3969/j.issn.1674-070X.2026.02.004 |
| 投稿时间：2025-09-22 |
| 基金项目:湖南省自然科学基金青年基金项目(2022JJ40240);湖南省卫生健康委科研计划项目一般资助课题(B202303067962);湖南省中医药研究院院联合基金项目(202126)。 |
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| Effects of Zicui Tongmai Drink on myocardial fibrosis in diabetic rats by regulating proinflammatory adipokines TNF-α, MCP-1, and PAI-1 |
| TAO Cuining, LUO Chunyu, LI Zhongxiao, ZHONG Conglu, ZHOU Wanying, BU Xianchun, TAN Jun, YUAN Chunyun |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Hunan Provincial Hospital of Integrated Traditional Chinese and Western Medicine/The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, Hunan, 410006, China) |
| Abstract: |
| Objective To investigate the effects of Zicui Tongmai Drink (ZCTMD) on myocardial fibrosis in diabetic rats by regulating the pro-inflammatory adipokines tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and plasmi-nogen activator inhibitor-1 (PAI-1). Methods Forty SD rats were selected, with 10 randomly assigned as the blank control group. The remaining 30 rats were used to establish a diabetic cardiomyopathy (DCM) model through a high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin (STZ). The successfully modeled rats were randomly divided into model group, ZCTMD group (17.6 g·kg-1) and enalapril group (0.53 mg·kg-1), with 9 rats in each group. Rats in each group were gavaged with the corre-sponding drugs once daily for 6 consecutive weeks. Body weight and fasting blood glucose (FBG) were regularly monitored before and after treatment. Biochemical methods were used to measure the levels of serum glucose (GLU), glycated serum protein (GSP), total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and lactate dehydrogenase (LDH) in rats. ELISA was employed to determine fasting insulin (FINS) levels, and the insulin resistance index (HOMA-IR) and insulin sensitivity index (ISI) were calculated. ELISA was also used to measure the levels of creatine kinase isoenzyme MB (CK-MB), cardiac troponin T (cTnT), type I collagen (COL-I), TNF-α, MCP-1, and PAI-1. Pathological and morphological changes in the myocardial tissue of DCM rats were observed through HE staining, Masson staining, and Sirius red staining, and the myocardial collagen volume fraction (CVF) level in the myocardial tissue of rats was calculated. Results Compared with the blank control group, the model group showed a decrease in body weight (P<0.01), and increases in FBG, GLU, GSP, TC, TG, LDL-C, HOMA-IR, LDH, CK-MB, cTnT, COL-Ⅰ, TNF-α, MCP-1, and PAI-1 levels (P<0.01), while FINS and ISI decreased (P<0.01). The myocardial tissue structure of rats in the model group was disorganized, with widened myocardial fiber gaps accompanied by collagen deposition, fatty degeneration of myocardial cells, infiltration of inflammatory cells, and an increased CVF (P<0.01). Compared with the model group, the ZCTMD group showed an increase in body weight (P<0.05) and decreases in FBG, GLU, GSP, TC, TG, LDL-C, HOMA-IR, LDH, CK-MB, cTnT, COL-Ⅰ, TNF-α, MCP-1, and PAI-1 (P<0.05, P<0.01), while FINS and ISI increased (P<0.05, P<0.01). The myocardial fibers in rats in the ZCTMD group were arranged more neatly, myocardial cell morphology tended to be normal, inflammatory infiltration alleviated, and CVF decreased (P<0.01). Conclusion ZCTMD can improve myocardial fibrosis in DCM rats, and its mechanism of action may be related to down-regulating the release of pro-inflammatory adipocytokines TNF-α, MCP-1, and PAI-1, thereby inhibiting myocardial fibrosis. |
| Key words: diabetic cardiomyopathy myocardial fibrosis Zicui Tongmai Drink proinflammatory adipokines tumor necrosis factor-α monocyte chemoattractant protein-1 plasminogen activator inhibitor-1 |
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