Fasudil alleviates hepatic fibrosis in type 1 diabetic rats: involvement of the inflammation and RhoA/ROCK pathway

European Review for Medical and Pharmacological Sciences
Y XieLi Chu

Abstract

Rho-associated kinases (ROCKs) are recognized to be involved in many pathophysiological processes caused by hyperglycemia. We performed experiments to evaluate the effects of fasudil, the Rho/ROCK inhibitor, on preventing hepatic fibrosis in type 1 diabetic rats and to elucidate the underlying mechanisms. Sprague-Dawley (SD) rats were randomly divided into five groups: normal control (NC), untreated diabetic (DM), low-dose fasudil-treated (L-Fas), high-dose fasudil-treated (H-Fas) and captopril-treated (Cap) groups. Streptozotocin was injected to establish the diabetes model. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), were analyzed. Hematoxylin and eosin (HE) and Masson's trichrome staining were used for histological observations. The expression of transforming growth factor-β (TGF-β1), metalloproteinase-9 (MMP-9)/tissue inhibitor of metalloproteinase-1 (TIMP-1), collagen type Iα (Coll α1), nuclear factor-kappa B (NF-κB) and ROCK-1 were measured to investigate the mechanisms involved in fibrosis. The DM group exhibited hepatic fibrosis with remarkable liver damage and inflammation reaction by the activation of the NF...Continue Reading

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