Abstract:Objective To observe the antiviral action and mechanism of Kujin Tablets by stimulating RAW264.7 with Poly (I∶C) in vitro to simulate virus infection. Methods Cells were divided into control group, Poly (I∶C) group and Kujin Tablets group (1 mg/ml). The Poly (I∶C) group was stimulated with 20 μg/ml of Poly (I∶C) for 12 h, after Poly (I∶C) stimulation, the Kujin Tablets group was treated with the Kujin Tablets (1 mg/ml) for 6 h, while the control group received no special treatment. Antiviral factors (Toll-like receptor 3 [TLR3], interferon regulatory factor-3 [IRF3], interferon-β [IFN-β], interferon stimulated gene 15 [ISG15], oligosadenylate synthase 1[OAS1], myxovirus resistance 1 [MX1]), inflammatory factors (interleukin-6 [IL-6], tumor necrosis factor -α [TNF-α], transforming growth factor -β [TGF-β], endoplasmic reticulum stress gene (inositol-requiring enzyme 1α [IRE1α], spliced X-box binding protein 1 [xBP1s], and C/EBP homologous protein [CHOP]) mRNA levels; and IL-6, TNF-α, xBP1s, and caspase-3 protein levels were detected in all groups. Results The mRNA expression levels of TLR3, IRF3, IFN-β, ISG15, OAS1, MX1, IL-6, TNF-α, TGF-β, IRE1α, xBP1s, and CHOP in Poly (I∶C) group were higher than those in control group, and the differences were statistically significant (P < 0.05). Compared with Poly (I∶C) group, the mRNA expression levels of TLR3, IRF3, IFN-β, ISG15, OAS1, and MX1 in Kujin Tablets group were up-regulated, while the mRNA expression levels of IL-6, TNF-α, TGF-β, IRE1α, xBP1s, and CHOP were down-regulated, and the differences were statistically significant (P < 0.05). The protein expression levels of IL-6, TNF-α, xBP1s, and caspase-3 in Poly (I∶C) group were higher than those in control group, and the differences were statistically significant (P < 0.05). The protein expression levels of IL-6, TNF-α, xBP1s, and caspase-3 in Kujin Tablets group were lower than those in Poly (I∶C) group, and the differences were statistically significant (P < 0.05). Conclusion Kujin Tablets can reduce virus-induced apoptosis, and its mechanism is related to promoting intrinsic antiviral response, reducing the release of inflammatory mediators and regulating endoplasmic reticulum stress.