{Reference Type}: Journal Article
{Title}: Fangchinoline induces antiviral response by suppressing STING degradation.
{Author}: Wang J;Xie F;Jia X;Wang X;Kong L;Li Y;Liang X;Zhang M;He Y;Feng W;Luo T;Wang Y;Xu A;
{Journal}: J Pharm Anal
{Volume}: 14
{Issue}: 6
{Year}: 2024 Jun
{Factor}: 14.026
{DOI}: 10.1016/j.jpha.2024.100972
{Abstract}: The stimulator of interferon genes (STING), an integral adaptor protein in the DNA-sensing pathway, plays a pivotal role in the innate immune response against infections. Additionally, it presents a valuable therapeutic target for infectious diseases and cancer. We observed that fangchinoline (Fan), a bis-benzylisoquinoline alkaloid (BBA), effectively impedes the replication of vesicular stomatitis virus (VSV), encephalomyocarditis virus (EMCV), influenza A virus (H1N1), and herpes simplex virus-1 (HSV-1) in vitro. Fan treatment significantly reduced the viral load, attenuated tissue inflammation, and improved survival in a viral sepsis mouse model. Mechanistically, Fan activates the antiviral response in a STING-dependent manner, leading to increased expression of interferon (IFN) and interferon-stimulated genes (ISGs) for potent antiviral effects in vivo and in vitro. Notably, Fan interacts with STING, preventing its degradation and thereby extending the activation of IFN-based antiviral responses. Collectively, our findings highlight the potential of Fan, which elicits antiviral immunity by suppressing STING degradation, as a promising candidate for antiviral therapy.