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. 2023 Nov 2;9(11):e21522.
doi: 10.1016/j.heliyon.2023.e21522. eCollection 2023 Nov.

Shengmai injection inhibits palmitic acid-induced myocardial cell inflammatory death via regulating NLRP3 inflammasome activation

Gang Yin  1 , Zi-Qing Hu  1 , Jing-Ya Li  1 , Zhong-Yu Wen  1 , Yong-Qin Du  1 , Peng Zhou  1   2 , Liang Wang  1   2
Affiliations

Shengmai injection inhibits palmitic acid-induced myocardial cell inflammatory death via regulating NLRP3 inflammasome activation

Gang Yin et al. Heliyon. .

Abstract

Objective: To determine the protective effect of Shengmai injection (SMI) on myocardial injury in diabetic rats and its mechanism based on NLRP3/Caspase1 signaling pathway.

Materials and methods: Rat H9c2 cardiomyocytes were cultured in vitro, and the cell survival rate of different concentrations of palmitate acid (PA) and different concentrations of SMI were detected by CCK-8. The myocardial injury cell model was induced with PA, treated with SMI, and combined with NLRP3 specific inhibitor (MCC950) to interfere with the high-fat-induced rat H9c2 myocardial cell injury model. The cell changes were observed by Hoechst/PI staining and the expression levels of MDA, SOD, and ROS in each group were detected. The protein and gene changes of the NLRP3/Caspase-1 signaling pathway were detected by Western blot and RT-qPCR, respectively.

Results: 200 μmol/L of PA were selected to induce the myocardial injury cell model and 25 μL/mL of SMI was selected for intervention concentration. SMI could significantly reduce MDA expression, increase SOD level, and decrease ROS production. SMI could decrease the gene expression levels of NLRP3, ASC, Caspase-1, and GSDMD, and the protein expressions of NLRP3, ASC, Cleaved Caspase-1, GSDMD, and GSDMD-N.

Conclusion: SMI can inhibit the high-fat-induced activation of the NLRP3/Caspase-1 signaling pathway, intervene in cardiomyocyte pyroptosis, and prevent diabetic cardiomyopathy.

Keywords: Diabetic cardiomyopathy; NLRP3/Caspase-1 signaling pathway; Pyroptosis; Shengmai injection.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Effect of different concentrations of PA on the viability of H9c2 cells **P < 0.01 vs control group.
Fig. 2
Fig. 2
Effect of different concentrations of SMI on viability of H9c2 cells **P < 0.01 vs control group.
Fig. 3
Fig. 3
Effect of SMI on MDA and SOD levels in H9c2 cells in each group. (A) The MDA expression levels in H9c2 cells. (B) The SOD expression levels in H9c2 cells. **P < 0.01 vs control group; ##P < 0.01 vs PA group.
Fig. 4
Fig. 4
Effect of SMI on ROS level in H9c2 cells in each group (100 × ). **P < 0.01 vs control group; ##P < 0.01 vs PA group.
Fig. 5
Fig. 5
Effect of SMI on pyroptosis in H9c2 cells (100 × ) **P < 0.01 vs control group; ##P < 0.01 vs PA group.
Fig. 6
Fig. 6
The effect of SMI on the level of genes related to PA-induced pyroptosis. (A) The mRNA expression of NLRP3 in H9c2 cells. (B) The mRNA expression of ASC in H9c2 cells. (C) The mRNA expression of Caspase1 in H9c2 cells. (D) The mRNA expression of GSDMD in H9c2 cells. **P < 0.01 vs control group; ##P < 0.01 vs PA group.
Fig. 7
Fig. 7
Effect of SMI on the protein expression of the NLRP3/Caspase1 signaling pathway in PA-induced H9c2 cells. (A) The protein expression of NLRP3, GSDMD, Cleaved-caspase1, GSDMD-N and ASC in H9c2 cells. (B) The protein expression of NLRP3 in H9c2 cells. (C) The protein expression of ASC in H9c2 cells. (D) The protein expression of Cleaved-Caspase1 in H9c2 cells. (E) The protein expression of GSDMD in H9c2 cells. (F) The protein expression of GSDMD-N in H9c2 cells. **P < 0.01 vs control group; #P < 0.05, ##P < 0.01 vs PA group.
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