Bradykinin Protects Against Hepatic Fibrosis
May lead to new therapeutic approach for chronic liver disease
TUESDAY, Dec. 4 (HealthDay News) -- Bradykinin, the main effector of the kallikrein-kinin system (KKS), exerts a protective effect against hepatocyte damage and fibrosis in chronic liver disease, according to the results of a study published in the December issue of Gastroenterology.
Pau Sancho-Bru, of the Institut Clinic de Malalties Digestives I Metaboliques in Barcelona, Spain, and colleagues examined the KKS in cultured human hepatocytes and hepatic stellate cells (HSCs) using quantitative reverse-transcription polymerase chain reaction, immunohistochemistry and Western blotting. They also evaluated the effect of bradykinin infusion on liver injury in rats and mice treated with carbon tetrachloride and Fas-stimulating antibody, respectively.
The researchers detected both bradykinin and kallikrein-1 in normal and fibrotic human livers and hepatic stellate cells, with bradykinin receptors up-regulated in fibrotic livers and activated HSCs. They also found bradykinin infusion attenuated hepatic fibrosis, reduced hepatocellular apoptosis, and lowered serum markers for hepatocyte damage in mice and rats with liver injury.
"These results suggest that the KKS may be involved in the wound healing response to chronic injury and that bradykinin may exert hepatoprotective and antifibrogenic effects in chronic liver diseases," the authors conclude. "Our results also suggest a potential usefulness for exogenous bradykinin in the prevention of hepatocellular injury."
One of the study authors reports having had a fellowship from Bayer Healthcare, LLC.