关键词: 肺炎, 心肌, 人参皂甙类, Toll样受体4, NF-κB, 细胞凋亡

Abstract: Objective　To investigate the effect and mechanism of ginsenoside Rg1 on myocardial tissue injury in rats with severe pneumonia. Methods　A total of 40 rats were injected with Klebsiella pneumoniae solution into trachea to construct severe pneumonia model. The model rats were divided into model group and low, medium and high dose drug groups. Another 10 untreated rats were taken as control group. The rats in the low, medium and high dose drug groups were given ginsenoside Rg1 with 2.5, 5 and 10 mg/kg by gavage, while the rats in the model group and the control group were given the same amount of normal saline, once a day for 14 days. Hematoxylin eosin stain method was used to observe the pathological morphology of myocardial tissue in rats and integral statistics was performed. The left ventricular diastolic pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximal descending rate of left ventricular pressure (-dP/dtmax) and maximal developing rate of left ventricular pressure (+dP/dtmax) of rats were measured by color Doppler ultrasound. The serum contents of B-type natriuretic peptide (BNP), cardiac troponin I (cTnI) and MB isoenzyme of creatine kinase (CK-MB) were detected by enzyme-linked immunosorbent assay (ELISA).The mRNA expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α) were detected by real-time fluorescence quantitative PCR (qPCR). The protein expression levels of apoptosis-related protein cleaved cysteiny l aspartate specific proteinase 3 (cleaved caspase-3) and inactive state (procaspase-3), Bcl-2 and Bcl-2 associated X protein (Bax), Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-κB (NF-κB) p65 and phosphorylated (p)-NF-κB p65 in myocardial tissue were detected by Western blot assay. Results　The myocardial tissue structure was normal in the control group, and the central muscle cells of the model group were disorderly arranged and swelled, and the muscle fibers were partially broken and accompanied with inflammatory cell infiltration. Compared with the model group, the morphological changes of myocardial cells were significantly improved in low, medium and high dose drug groups. Compared with those in the control group, the pathological score, LVEDP level, BNP, cTnI, CK-MB contents, IL-6, IL-1β, TNF-α mRNA levels, cleaved caspase-3/procaspase-3, Bax/Bcl-2 ratio and TLR4, MyD88, p-NF-κB p65 protein expression levels were significantly higher in the model group, while the levels of LVDP, -dP/dtmax and +dP/dtmax were significantly lower (P＜0.05). After intragastric administration of ginsenoside Rg1, the above changes induced by modeling were reversed in a dose-dependent manner (P＜0.05). Conclusion　Ginsenoside Rg1 can protect severe pneumonia rats from myocardial tissue injury by reducing inflammatory reaction and myocardial apoptosis, and its mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway activation.

Key words: pneumonia, myocardium, ginsenosides, Toll-like receptor 4, NF-kappa B, apoptosis