Abstract: This study observes the therapeutic detoxification of quercetin, a well-known flavonoid, against carbon tetrachloride (CCl₄) induced acute liver injury in vivo and explores its mechanism. Quercetin decreased CCl₄-increased serum activities of alanine and aspartate aminotransferases (ALT/AST) when orally taken 30 min after CCl₄ intoxication. The results of a histological evaluation further evidenced the ability of quercetin to protect against CCl₄-induced liver injury. Quercetin decreased the CCl₄-increased malondialdehyde (MDA) and reduced the glutathione (GSH) amounts in the liver. It also reduced the enhanced immunohistochemical staining of the 4-hydroxynonenal (4-HNE) in the liver induced by CCl₄. Peroxiredoxin (Prx) 1, 2, 3, 5, 6, thioredoxin reductase 1 and 2 (TrxR1/2), thioredoxin 1 and 2 (Trx1/2), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) all play critical roles in maintaining cellular redox homeostasis. Real-time polymerase chain reaction (PCR) results demonstrated that quercetin reversed the decreased mRNA expression of all those genes induced by CCl₄. In conclusion, our results demonstrate that quercetin ameliorates CCl₄-induced acute liver injury in vivo via alleviating oxidative stress injuries when orally taken after CCl₄ intoxication. This protection may be caused by the elevation of the antioxidant capacity induced by quercetin.

Key words: Hepatotoxicity, Oxidative stress, Peroxiredoxin (Prx), Nuclear factor erythroid 2-related factor 2 (Nrf2), TrxR, Trx, HO-1

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