Shenge powder inhibits myocardial fibrosis in rats with post-myocardial infarction heart failure through LOXL2/TGF-β1/IL-11 signaling pathway.
10.3724/zdxbyxb-2024-0606
- Author:
Hang XIE
1
,
2
;
Boyong QIU
3
;
Haitao LI
4
;
Ruoyu SHI
5
Author Information
1. Department of Critical Care Medicine, Henan Provincial Hospital of Traditional Chinese Medicine (the Second Affiliated Hospital of Henan University of Chinese Medicine), Zhengzhou 450053, China. 15003892657@
2. com.
3. Heart Center, the First Affiliated Hospital of Henan University of Chinese Medicine,National Regional Traditional Chinese Medicine (Cardiovascular) Diagnosis and Treatment Center, Zhengzhou 450099, China. 1057180884@qq.com.
4. Heart Center, the First Affiliated Hospital of Henan University of Chinese Medicine,National Regional Traditional Chinese Medicine (Cardiovascular) Diagnosis and Treatment Center, Zhengzhou 450099, China.
5. Department of Nephrology, Henan Provincial Hospital of Traditional Chinese Medicine (the Second Affiliated Hospital of Henan University of Chinese Medicine), Zhengzhou 450053, China］.
- Publication Type:Journal Article
- Keywords:
Fibrosis;
Heart failure;
LOXL2/ TGF-β1/IL-11 signaling pathway;
Myocardial infarction;
SD rats;
Shenge powder
- MeSH:
Animals;
Male;
Rats, Sprague-Dawley;
Myocardial Infarction/complications*;
Transforming Growth Factor beta1/metabolism*;
Signal Transduction/drug effects*;
Drugs, Chinese Herbal/therapeutic use*;
Rats;
Heart Failure/pathology*;
Myocardium/metabolism*;
Fibrosis;
Amino Acid Oxidoreductases/metabolism*;
Interleukin-11/metabolism*;
Tissue Inhibitor of Metalloproteinase-1/metabolism*;
Matrix Metalloproteinase 9/metabolism*
- From:
Journal of Zhejiang University. Medical sciences
2025;54(3):350-359
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the effect of Shenge powder (SGP) on myocardial fibrosis in rats with heart failure after myocardial infarction and its relation with lysyl oxidase like protein 2 (LOXL2)/transforming growth factor-β1 (TGF-β1)/IL-11 signaling pathway.
METHODS:Seventy-two SPF male SD rats were divided into blank control group, model control group, SGP small dose group, SGP large dose group, positive control group, SGP large dose+LOXL2 activator group, with 12 rats in each group. Except for the blank control group, post-myocardial infarction heart failure was induced by coronary constriction. Corresponding treatments were given immediately after successful modeling, once a day for 4 weeks. Left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) in rats were detected by color Doppler ultrasound imaging. Levels of IL-1β and IL-6 in serum were analyzed by ELISA method. Myocardial collagen volume fraction (CVF) was evaluated by Masson staining. Expressions of collagen Ⅰ and α-smooth muscle actin (α-SMA) in myocardial tissue were detected by immunohistochemical staining. The mRNA expressions of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in myocardial tissue were detected by qRT-PCR. Expression of LOXL2, TGF-β1, and IL-11 proteins in myocardial tissue were detected by Western blotting.
RESULTS:Compared with the blank control group, the LVFS and LVEF of the model control group decreased, the levels of serum IL-6 and IL-1β elevated, and the CVF value, the expressions of collagen Ⅰ and α-SMA in myocardial tissue, MMP-9 and TIMP-1 mRNA, and LOXL2, TGF-β1, IL-11 proteins increased (all P<0.05). Compared with the model control group, the LVFS and LVEF of SGP small dose group, SGP large dose group and positive control group increased, the levels of serum IL-6 and IL-1β decreased, and the CVF value, the expressions of collagen Ⅰ and α-SMA in myocardial tissue, MMP-9 and TIMP-1 mRNA, and LOXL2, TGF-β1, IL-11 proteins decreased (all P<0.05); while LOXL2 activator reversed the improvement effect of high-dose SGP on myocardial fibrosis in heart failure rats after myocardial infarction.
CONCLUSIONS:Shenge powder may inhibit myocardial fibrosis in heart failure rats after myocardial infarction by inhibiting the LOXL2/TGF-β1/IL-11 pathway.
