Applied Sciences (Apr 2023)

Hepatoprotective Effect of Alpinetin on Thioacetamide-Induced Liver Fibrosis in Sprague Dawley Rat

  • Suhayla Hamad Shareef,
  • Ameena S. M. Juma,
  • Derin N. F. Agha,
  • Abdullah R. Alzahrani,
  • Ibrahim Abdel Aziz Ibrahim,
  • Mahmood Ameen Abdulla

DOI
https://doi.org/10.3390/app13095243
Journal volume & issue
Vol. 13, no. 9
p. 5243

Abstract

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Alpinetin is an original medicinal plant flavonoid derived from Alpinia katsumadai and has several biological activities. The current research aimed to evaluate the hepatoprotective effects of Alpinetin against thioacetamide (TAA)-induced liver cirrhosis in rats. Five groups of rats were utilized in this study. Hepatic injury was measured macroscopically and microscopically for entire groups. The rats’ body weight was significantly lower in the TAA control group, likened to rats fed with Silymarin or Alpinetin groups, while liver weight was significantly greater in the TAA control group when equated to rats nourished with Alpinetin groups. A histopathological investigation of hepatic tissues displayed that TAA remarkably induced hepatocyte necrosis and gristly connective tissue propagation in the TAA control group. Alpinetin implicitly decreased the influence of TAA toxicity and diminished fibrosis of liver tissues. The TAA control group presented an increase in liver enzymes (ALP, ALT, and AST) and a decrease in total protein and albumin. Rats who were fed Alpinetin had significantly lower hepatic enzyme activity as well as augmented total protein and albumin, yet they were close to the normal range. Superoxide dismutase (SOD) and Catalase (CAT) enzymes in hepatic homogenate were significantly reduced, and malondialdehyde (MDA) was meaningfully elevated in the TAA control group, while rats fed with Alpinetin had significantly increased SOD and CAT achievement and depressed MDA level. Alpinetin-gavaged groups had reduced levels of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6), significantly down-regulated Proliferating cell nuclear antigen (PCNA), Alpha-smooth muscle (α-SMA), and reduced hepatic stellate cell activity. However, the TAA control group significantly up-regulated PCNA and α-SMA and increased the activity of hepatic stellate cells. Alpinetin was nontoxic and could improve defensive mechanisms against hepatic tissue injury. Acute toxicity tests discovered no evidence of any toxic signs or dead rats, which highlights the safety of Alpinetin. Consequently, the investigation´s outcomes revealed that the hepatoprotective effects of Alpinetin in TAA-induced hepatic impairment might be due to reduced TAA toxicity, increased protein and albumin, increased SOD and CAT levels, reduced MDA levels, and modulation of inflammatory cytokines and their anti-oxidant activities, and suppressed PCNA and α-SMA.

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