Taurocholic acid (TCA) sodium, a conjugation of cholic acid with taurine, is one of the main bile acids that is elevated in liver disease. In pretreated gingival fibroblasts and HSC-2 cells, TCA considerably reduced the expression of IL1β, IL6, and IL8. TCA has anti-inflammatory activity in gingival fibroblasts, human oral squamous cell carcinoma cells and macrophages in vitro[2]. TCA increased the expression of α-SMA, type I collagen, and TLR4 in LX-2 cells (Hepatic stellate cells). TCA promoting liver cirrhosis is likely through activating hepatic stellate cells via upregulating TLR4 expression[3]. An oral dosing of either acetylsalicylic acid (ASA) or taurocholic acid (TCA) to pylorus-ligated rats subjected to water-immersion stress produced severe damage to the gastric musoca in contrast to the irritation observed in non-stressed ones. The irritative activity of ASA or TCA on gastric mucosa under stress was dose-dependent[4]. Long-term supplementation with small doses of TCA was demonstrated to improve glucose metabolism in a diabetic rat model and may be a potential target for diabetes control[5].
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