The anti-inflammatory effect of Sheshang capsule on Trimeresurus stejnegeri bites based on miR-155/TLR4/MyD88

Wang Shijun; Shen Fanghua; Zhang Meiji; Zhan Xuejing; Wang Youqian; Cai Jiaqing; Lin Yili

doi:10.3969/j.issn.1002-1949.2024.05.005

Abstract：Objective To investigate the effects of Sheshang capsule on miR-155/Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)signaling pathway and the inflammation in Trimeresurus stejnegeri bites.Methods The 18 male New Zealand white rabbits were divided into control group,model group and Sheshang capsule group with 6 rabbits in each group.The rabbits in control group accepted normal diet and water.The model group was given intragastric infusion with 348 mg/(kg·d)normal saline and Sheshang capsule group was given intragastric infusion with 348 mg/(kg·d)Sheshang capsule for continous 7 days at 6 h after the infusion of 7.5 mg/kg Trimeresurus stejnegeri venom.The expressions of miR-146a-5p,TLR4 and MyD88 in peripheral blood were detected by reverse transcription quantitative real-time polymerase chain reaction(qRT-PCR),and the contents of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),interferon-γ(IFN-γ),and interleukin-4(IL-4)in serum were detected by enzyme-linked immunosorbent assay(ELISA).Results Compared with the control group,the spirit and appetite of the rabbits in model group became worse,the defecation was soft and bleeding,the wound festered,and the expressions of miR-155-5p,TLR4 mRNA,MyD88 mRNA,IL-6 and TNF-α were significantly increased(all P<0.01),and the expressions of IFN-γ and IL-4 were significantly decreased(all P<0.01).The rabbits in the Sheshang capsule group were significantly improved compared with the model group,and the expressions of miR-155-5p,TLR4 mRNA,MyD88 mRNA,IL-6 and TNF-α were significantly decreased(all P<0.01),while the expressions of IFN-γ and IL-4 were significantly increased(all P<0.01).Conclusions Sheshang capsule can inhibit the inflammatory response caused by Trimeresurus stejnegeri venom and maintain the balance of Th1/Th2 cells,and its mechanism may be related to the inhibition of miR-155/TLR4/MyD88 axis expression.