PM2.5 通过 Ang II/ERK1/2/TGF-β 信号通路诱导小鼠模型心肌纤维化。

PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β signaling pathway in mice model.

机构信息

Tianjin Medical University, Teda International Cardiovascular Hospital, Tianjin, China.

Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease(Key Lab-TIC), Tianjin Institute of Cardiology (TIC), Department of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China.

出版信息

J Renin Angiotensin Aldosterone Syst. 2021 Jan-Dec;22(1):14703203211003786. doi: 10.1177/14703203211003786.

OBJECTS

To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.

METHODS

PM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β was examined by Western Blotting (WB) and Real time PCR (RT-PCR).

RESULTS

The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β was increased in higher dose groups in protein and mRNA level.

CONCLUSION

PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.

目的

探讨 PM2.5 对心肌纤维化的影响及相关机制。

方法

将 PM2.5 颗粒制备成不同浓度的溶液，每周两次滴入小鼠气管。将小鼠分为五组：空白对照组（C 组）、NS 对照组（J 组）、高剂量组（G 组，10mg/kg）、中剂量组（Z 组，5mg/kg）和低剂量组（D 组，2.5mg/kg）。6 周后，通过 HE 和 Masson 染色观察心肌纤维化。通过 Western Blotting（WB）和 Real time PCR（RT-PCR）检测 Ang II、ERK1/2 和 TGF-β的表达。