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徐丹,董朝阳,郭睿,郭冰,毛以林.基于心康冲剂调控慢性心力衰竭大鼠JAK2/STAT3通路抗心肌纤维化的作用机制[J].湖南中医药大学学报英文版,2023,43(8):1388-1393.[Click to copy
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| 基于心康冲剂调控慢性心力衰竭大鼠JAK2/STAT3通路抗心肌纤维化的作用机制 |
| 徐丹,董朝阳,郭睿,郭冰,毛以林 |
| (湖南中医药大学, 湖南 长沙 410208;湖南中医药大学第二附属医院, 湖南 长沙 410005) |
| 摘要: |
| 目的 探讨心康冲剂抗慢性心力衰竭大鼠心肌纤维化的机制。方法 48只雄性SD大鼠随机均分为正常组、模型组、心康冲剂治疗组（治疗组）、缬沙坦对照组（缬沙坦组）。除正常组外，其余各组经腹腔注射注射用盐酸多柔比星1.5 mg/kg制造慢性心力衰竭大鼠模型。治疗组给与1.2 g/（kg·d）心康冲剂；缬沙坦组给与1.62 mg/（kg·d）缬沙坦胶囊；正常组、模型组给予等体积灭菌注射用水灌胃。每日1次，连续灌胃8周。以超声心动图检测大鼠心功能[左室射血分数（left ventricular ejection fractions，LVEF）、左心室短轴缩短率（left ventricular fractional shortening，LVFS）]，Masson染色观察心肌纤维化，RT-qPCR法检测心肌组织Ⅰ型胶原（collagen Ⅰ，ColⅠ）mRNA表达水平，Western blot法检测心肌ColⅠ、磷酸化酪氨酸激酶2（phospho-Janus kinase，p-JAK2）、磷酸化信号转导和转录激活子3（phoso-signal transducer and activator of transcription 3，p-STAT3）的蛋白含量。用Pearson相关及线性回归分析ColⅠ、p-JAK2、p-STAT3与左室收缩末期内径（left ventricular end systolic diameter，LVESD）之间的相关性。结果 与正常组比较，模型组大鼠LVEF、LVFS显著下降（P<0.01）；与模型组比较，治疗组大鼠LVEF、LVFS均升高（P<0.01），LVESD下降（P<0.01），ColⅠmRNA及蛋白含量均下降（P<0.05，P<0.01），p-JAK2、p-STAT3蛋白含量均下降（P<0.05，P<0.01）；与缬沙坦组比较，治疗组LVEF、LVFS升高（P<0.01），p-STAT3蛋白含量降低（P<0.05），而ColⅠmRNA、p-JAK2、ColⅠ蛋白含量差异无统计学意义（P>0.05）。ColⅠ、p-STAT3、p-JAK2均与LVESD具有明显线性关系。结论 心康冲剂可通过下调JAK2/STAT3信号通路激活，降低ColⅠmRNA表达与ColⅠ蛋白合成，从而抗慢性心力衰竭大鼠心肌纤维化。 |
| 关键词: 慢性心力衰竭 心康冲剂 心肌纤维化 JAK2/STAT3信号通路 Ⅰ型胶原 |
| DOI：10.3969/j.issn.1674-070X.2023.08.007 |
| Received:January 08, 2023 |
| 基金项目:湖南省自然科学基金项目（2020JJ4473）；湖南省中医药管理局重点科研项目（C2022004）；湖南中医药大学2022一方研究生创新项目（2022YF07）。 |
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| Mechanism of action of Xinkang Granule against myocardial fibrosis by regulating JAK2/STAT3 signaling pathway in rats with chronic heart failure |
| XU Dan,DONG Chaoyang,GUO Rui,GUO Bing,MAO Yilin |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;The Second Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410005, China) |
| Abstract: |
| Objective To investigate the mechanism of Xinkang Granule (XKG) against myocardial fibrosis in rats with chronic heart failure (CHF). Methods Forty-eight male SD rats were randomly divided into normal group, model group, XKG treatment group (treatment group), valsartan control group (valsartan group). Except for the normal group, the other groups were injected intraperitoneally with doxorubicin hydrochloride 1.5 mg/kg to establish a rat model of CHF. Then, the treatment group was given XKG 1.2 g/(kg·d) the valsartan group was given valsartan capsules 1.62 mg/(kg·d), and the normal group and the model group were given equal volumes of sterilized water for injection. All the rats received gavage once daily, continuously for 8 weeks. The cardiac functions of rats including left ventricular ejection fractions (LVEF) and left ventricular fractional shortening (LVFS) were measured by echocardiography, myocardial fibrosis was observed by Masson staining, the mRNA expression level of collagen Ⅰ (Col Ⅰ) in myocardial tissue was examined by RT-qPCR, and the protein level of myocardial ColⅠ, phospho-Janus kinase 2 (p-JAK2), phoso-signal transducer, and activator of transcription 3 (p-STAT3) were measured by Western blot. Moreover, Pearson's correlation and linear regression were used to analyze the correlation between ColⅠ, p-JAK2, p-STAT3, and left ventricular end systolic diameter (LVESD). Results Compared with the normal group, LVEF and LVFS in the model group significantly decreased (P<0.01); compared with the model group, LVEF and LVFS in the treatment group increased (P<0.01), LVESD decreased (P<0.01), and the mRNA expression and protein level of ColⅠ as well as the protein levels of p-JAK2 and p-STAT3 were reduced (P<0.05, P<0.01); compared with the valsartan group, LVEF and LVFS in the treatment group were higher (P<0.01), but the protein level of p-STAT3 was lower (P<0.05), and there was no significant difference in Col Ⅰ mRNA expression and the protein levels of p-JAK2 and Col Ⅰ(P>0.05). ColⅠ, p-STAT3, and p-JAK2 all had obvious linear relationships with LVESD. Conclusion XKG can inhibit myocardial fibrosis in rats with chronic heart failure by down-regulating the activation of JAK2/STAT3 signaling pathway and reducing the mRNA expression and protein synthesis of ColⅠ. |
| Key words: chronic heart failure Xinkang Granule myocardial fibrosis JAK2/STAT3 signaling pathway collagenⅠ |
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