Tannic acid alleviates experimental pulmonary fibrosis in mice by inhibiting inflammatory response and fibrotic process

Hydrolysable tannins as a potential therapeutic drug for the human fibrosis‐associated disease

“…Macrophages exert bidirectional functions in the regulation of matrix deposition and resolution in fibrotic disease, but M1 polarized macrophages induced fibrosis by promoting the process of EMT (Ma et al, 2017). Similarly, the research team (Rajasekar et al, 2020) showed that HT-inhibited polarized macrophage-induced EMT and diminished activation of MAPK in lung epithelial cells. The mechanism for suppressing EMT in cells could directly bind toll-like receptor 4 (TLR4) to inhibit the formation of the LPS-TLR4/MD2 complex and block of subsequent downstream signal transduction .…”

“…A few studies have indicated that HT displayed therapeutic potential against pulmonary fibrosis in multiple ways. For instance, Rajasekar et al (2020) reported that treatment with HT significantly ameliorated histological injury, reduced inflammatory cell infiltration, and decreased the levels of various inflammatory mediators in the lungs of mice. HT also inhibited the expression of profibrotic and fibrotic markers, including transforming growth factor-β1 (TGF-β1), collagen 1 alpha and fibronectin, and suppressed the phosphorylation of extracellular signal-regulated kinase 1/2 (Erk1/2) in a bleomycin-induced pulmonary fibrosis model.…”

“…The mechanism for suppressing EMT in cells could directly bind toll-like receptor 4 (TLR4) to inhibit the formation of the LPS-TLR4/MD2 complex and block of subsequent downstream signal transduction . The research team (Rajasekar et al, 2020) have markedly reported that HT could alleviate pulmonary fibrosis via inhibiting profibrotic process and EMT in vivo or in vitro model of fibrosis from three studies. Furthermore, Reed et al (2019) The research reported that HT-induced hydrogen peroxide production triggers as an initiator of c-jun N-terminal kinase signaling pathways and it leads to apoptosis in mouse lung fibroblasts (Chen et al, 2013).…”

“…This process accelerates the T A B L E 3 Antifibrotic effects of hydrolyzed tannins in cardiac fibrosis and other fibrotic diseases. fibrosis (Chu et al, 2016;Du et al, 2016;Go et al, 2016;Huang et al, 2013;Li et al, 2016;Rajasekar et al, 2020;Rong et al, 2018). By modulating macrophages polarization, HT inhibited LPS-induced M1 macrophages polarization in lung epithelial cells and decreased the activation of M1 macrophages in the hepatic mononuclear cells to alleviate fibrosis (Du et al, 2016;Li et al, 2017;Yan et al, 2021).…”

“…Numerous studies have reported that HT exhibits therapeutic effects on fibrotic diseases by inhibiting inflammatory response and fibrotic process, reducing collagen accumulation and oxidative stress, and preventing macrophage‐induced profibrotic response. These findings suggest that HT have the potential to serve as alternative drugs for preventing the development of organ fibrosis (Chu et al, 2016; Ma et al, 2020; Rajasekar et al, 2020). Therefore, in this review, we described the pharmacological mechanisms of HT in the prevention and treatment of fibrotic diseases in main organs and provided new insight into the alternative drugs for antifibrosis in clinical application.…”