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Hepatoprotectivity of Panduratin A against liver damage: In vivo demonstration with a rat model of cirrhosis induced by thioacetamide
Author(s) -
Salama Suzy M.,
Ibrahim Ibrahim Abdel Aziz,
Shahzad Naiyer,
AlGhamdi Saeed,
Ayoub Nahla,
AlRashdi Ahmed Salim,
Abdulla Mahmood Ameen,
Salehen Nur'Ain,
Bilgen Mehmet
Publication year - 2018
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12878
Subject(s) - thioacetamide , chemistry , oxidative stress , alkaline phosphatase , alanine transaminase , malondialdehyde , in vivo , aspartate transaminase , hepatic stellate cell , cirrhosis , medicine , pharmacology , nitrotyrosine , endocrinology , biochemistry , biology , enzyme , nitric oxide synthase , microbiology and biotechnology
This experiment evaluated Panduratin A ( PA ), a chalcone isolated from Boesenbergia rotunda rhizomes, for its hepatoprotectivity. Rats were subjected to liver damage induced by intra‐peritoneal injection of thioacetamide ( TAA ). PA was tested first for its acute toxicity and then administered by oral gavage at doses 5, 10, and 50 mg/kg to rats. At the end of the 8 th week, livers from all rats were excised and evaluated ex vivo . Measurements included alkaline phosphatase ( AP ), alanine transaminase ( ALT ), aspartate transaminase ( AST ) and gamma‐glutamyl transferase ( GGT ), serum platelet‐derived growth factor ( PDGF ) and transforming growth factor ( TGF ‐β1), and hepatic metalloproteinase enzyme ( MMP ‐2) and its inhibitor extracellular matrix protein ( TIMP ‐1). Oxidative stress was measured by liver malondialdehyde ( MDA ) and nitrotyrosine levels, urinary 8‐hydroxy 2‐ deoxyguanosine (8‐ OH ‐ dG ), and hepatic antioxidant enzyme activities. The immunohistochemistry of TGF ‐β 1 was additionally performed. PA revealed safe dose of 250 mg/kg on experimental rats and positive effect on the liver. The results suggested reduced hepatic stellate cells ( HSC s) activity as verified from the attenuation of serum PDGF and TGF ‐β1, hepatic MMP ‐2 and TIMP ‐1, and oxidative stress. The extensive data altogether conclude that PA treatment could protect the liver from the progression of cirrhosis through a possible mechanism inhibiting HSC s activity.