Bacterial protease alleviate chronic liver fibrosis induced by thioacetamide through suppression of hepatic stellate

Gad Elsayed Mohamed Salem1, Shaimaa M Azzam2, Mona A F Nasser3

  • 1Reef Biology Research Group, Department of Marine Science, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand.

Insights

Bacterial Protease (BP) shows protective potential against liver fibrosis by reducing inflammation and oxidative stress. This study suggests BP could be a valuable adjuvant therapy for treating liver fibrosis.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hepatology

Background:

  • Chronic liver diseases lead to liver fibrosis due to excessive extracellular matrix accumulation, causing millions of deaths annually.
  • Cirrhosis is a significant cause of mortality, necessitating novel therapeutic compounds for chronic liver disease management.
  • This study investigates the therapeutic potential of Bacterial Protease (BP) and a novel triazole compound (DPET) against liver fibrosis.

Purpose of the Study:

  • To evaluate the anti-inflammatory and antioxidant effects of Bacterial Protease (BP) and DPET in an early-stage liver fibrosis model.
  • To assess the impact of BP and DPET on liver function markers, oxidative stress, and inflammatory pathways.
  • To determine the efficacy of BP in mitigating thioacetamide-induced liver fibrosis and histopathological damage.

Main Methods:

  • Liver fibrosis was induced in male rats using thioacetamide (TAA).
  • Animals were divided into six groups: control, BP, TAA, TAA-Silymarin, TAA-BP, and TAA-DPET.
  • Key biomarkers including liver enzymes (ALT, AST, ALP), inflammatory cytokines (IL-6, VEGF), oxidative stress markers (MDA, SOD, NO, GSH), and gene expression (MAPK, MCP-1, Nrf2) were analyzed.

Main Results:

  • TAA-induced liver fibrosis significantly elevated liver enzymes, IL-6, VEGF, MDA, SOD, and NO, while decreasing GSH.
  • TAA treatment led to MAPK and MCP-1 upregulation, Nrf2 downregulation, and significant histopathological damage, including collagen deposition.
  • Bacterial Protease (BP) treatment ameliorated TAA-induced liver damage, improved histological architecture, and reduced fibrosis markers.

Conclusions:

  • Bacterial Protease (BP) demonstrates significant protective effects against liver fibrosis.
  • BP effectively attenuates inflammation and oxidative stress associated with liver fibrosis.
  • BP shows potential as an adjuvant therapy for managing hepatic fibrosis.

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