Aims: This study was designed to investigate the molecular mechanisms underlying the anti-inflammatory and anti-fibrosis effects of Berberine hydrochloride (BBR) following canalicular laceration (CL) surgical repair.
Main methods: We used a rabbit CL model in this study. BBR and the control medicine were administered during and after the surgical operation. The degree of fibrosis in the canaliculi was evaluated using hematoxylin and eosin and Masson's trichrome staining 7 days after the operation. Inflammation inside the canaliculi was observed using a transcanalicular endoscope. Expression levels of inflammatory cell cytokines [tumor growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), intracellular adhesion molecule-I (ICAM-1), and interleukin-β1 (IL-1β)] were detected using immunohistochemistry. P38 and ERK1 phosphorylation and activation were determined using western blot analysis.
Key findings: The degree of inflammation and fibrosis were less in the BBR groups compared to Surgery group. The anti-inflammatory and anti-fibrosis effects of BBR were concentration-dependent. The levels of TGF-β1, CTGF, ICAM-1, and IL-1β were significantly lower in the BBR groups compared to Surgery group. BBR reduced the phosphorylation of P38 compared to Surgery group.
Significance: In conclusion, this study shows that BBR can reduce local fibrosis after CL surgical repair via its anti-inflammatory and anti-fibrosis effects.
Keywords: Anti-fibrosis; Anti-inflammatory; Berberine hydrochloride; Canalicular laceration.
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