Baicalin suppresses expression of TLR2/4 and NF-κB in chlamydia trachomatis–infected mice

Abstract

Our previous studies have shown that the baicalin could blocked infection of chlamydia trachomatis (C. trachomatis)–infected cells in vitro. Toll-like receptor 2 and 4 (TLR2/4) and the downstream nuclear factor-κB (NF-κB) signaling pathway, which mediate the inflammatory reaction, are involved in the pathophysiological processes of inflammation. In this study, we investigated whether baicalin inhibits TLR2/4 signaling pathway in gential tract chlamydia–infected mice. The progesterone-treated animals were given intravaginally 200 mg/kg baicalin administered. Nineteen days after infection, cervical tissue were taken and expression of TLR2/4, NF-κB were determined by RT-PCR or westernblot. Nitric oxide and prostaglandin E2 production in cervical tissue were detected by enzyme-linked immunosorbent assay. It was demonstrated that baicalin significantly reduced C. trachomatis loading in BALB/c mice that were vaginally infected with the pathogen. Meanwhile, baicalin also reduced the expression of TLR2/4 and NF-κB, decreased activity of inducible nitric oxide synthase and cyclooxgenase-2 in cervical tissue. Our results suggest that baicalin inhibits the TLR2/4 signaling pathway in cervical tissue of gential tract chlamydia–infected mice. On the basis of these data and our previous observations, we conclude that further evaluation of baicalin for prevention and treatment of sexually transmitted chlamydial infection is warranted.

Keywords::

• Baicalin
• chlamydia trachomatis
• toll-like receptor
• nuclear factor-κB
• chlamydia-infected mice