This study observes the therapeutic detoxification of quercetin, a well-known flavonoid, against carbon tetrachloride (CCl 4 ) induced acute liver injury in vivo and explores its mechanism. Quercetin decreased CCl 4 -increased serum activities of alanine and aspartate aminotransferases (ALT/AST) when orally taken 30 min after CCl 4 intoxication. The results of a histological evaluation further evidenced the ability of quercetin to protect against CCl 4 -induced liver injury. Quercetin decreased the CCl 4 -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 CCl 4 . 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 CCl 4 . In conclusion, our results demonstrate that quercetin ameliorates CCl 4 -induced acute liver injury in vivo via alleviating oxidative stress injuries when orally taken after CCl 4 intoxication. This protection may be caused by the elevation of the antioxidant capacity induced by quercetin.
A simple, highly sensitive, specific, reproducible, and high-throughput Amide-HILIC-MS/MS assay to quantify metformin in rat plasma was established and successfully applied for sample analysis to support pharmacokinetic studies.
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