Key result
QiShenYiQi pill reduces myocardial collagen expression and cardiomyocyte apoptosis in experimental autoimmune cardiomyopathy.
Why the study?
QiShenYiQi pill has a myocardial protective effect, but its impact on myocardial collagen metabolism and apoptosis mechanisms in autoimmune cardiomyopathy required exploration.
Does QiShenYiQi pill reduce myocardial collagen deposition and apoptosis in a rat model of autoimmune cardiomyopathy?
Does QiShenYiQi pill reduce myocardial collagen deposition and apoptosis in a rat model of autoimmune cardiomyopathy?
QSYQ attenuates myocardial fibrosis and apoptosis in an experimental model of autoimmune cardiomyopathy, suggesting a potential therapeutic option for the disease.
Answers are grounded in this paper and cite their sources.
Should not yet inform clinical practice; hypothesis-generating for antifibrotic effects of QiShenYiQi in autoimmune cardiomyopathy.
CONTEXT: QiShenYiQi pill (QSYQ) is a traditional Chinese medicine with a myocardial protective effect. OBJECTIVE: To explore the effect of QSYQ on myocardial collagen metabolism in rats with autoimmune cardiomyopathy and explore the underlying mechanism from the aspect of apoptosis. MATERIALS AND METHODS: We established an autoimmune cardiomyopathy model using Lewis rats. The rats were then randomly divided into six groups (n = 8): control, model, 3-methyladenine (15 mg/kg, intraperitoneal injection), QSYQ low-dose (135 mg/kg, gavage), QSYQ medium dose (270 mg/kg, gavage), and QSYQ high-dose (540 mg/kg, gavage) for four weeks. Van Gieson staining was applied for myocardial pathological characteristics, TUNEL fluorescence for myocardial cell apoptosis, enzyme-linked immunosorbent assay (ELISA) for serum PICP, PIIINP, and CTX-I levels, and western blot analysis for type I/III myocardial collagen, Bcl-2, Bax, and caspase-3 proteins. RESULTS: Results showed that QSYQ (135, 270, or 540 mg/kg) significantly reduced the expression of myocardial type I/III collagen, and concentrations of serum PICP, PIIINP, and CTX-I in rats. Moreover, QSYQ could alleviate myocardial fibrosis more effectively at a higher dose. QSYQ could also inhibit myocardial apoptosis via downregulating Bcl-2 expression, and upregulating Bax and caspase-3 expression levels. DISCUSSION AND CONCLUSIONS: The QSYQ can improve myocardial collagen metabolism by inhibiting apoptosis, which provides a potential therapeutic approach for autoimmune cardiomyopathy.
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Lv et al. (2022) studied Autoimmune cardiomyopathy (n=48). QiShenYiQi pill vs. Distilled water (model group) and 3-methyladenine (active control) was evaluated on Myocardial type I/III collagen expression and apoptosis rate (p=<0.01). QiShenYiQi pill significantly reduced myocardial collagen expression and cardiomyocyte apoptosis compared to control in a rat model of autoimmune cardiomyopathy (p<0.01).
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