Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 120, Issue 8, Pages 12677-12683Publisher
WILEY
DOI: 10.1002/jcb.28535
Keywords
hepatoprotection; inflammation; liver; spleen; total flavonoids
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Funding
- \Guangxi Education Department Research Project [KY2015YB235]
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Hepatic function is of great concern in metabolic and immunological homeostasis. Traditionally, medical management to liver damage may benefit from phytomedicine, such as Chinese herbs. In southern China, Polygonum perfoliatum L can contribute to alleviating pathological symptoms of liver disease, such as hepatitis. However, bioactive compounds of hepatoprotection in this herb are still less to be investigated. In this study, clinical data of patients with drug-induced liver injury were collected on the basis of serological analyses. In addition, we extracted and identified total flavonoids from Polygonum perfoliatum L (TFPPL) before implementing biochemical experiments in vivo. In human data, the blood contents of liver function enzymes were visibly elevated, and the percentage of immune cells were abnormally changed. The data from the animal study showed that TFPPL-treated carbon tetrachloride-exposed mice resulted in reduced absolute liver mass and lowered blood levels of liver functional enzymes (alanine transaminase and aspartate transaminase). In enzyme-linked immunosorbent assay, the comparable data indicated that serological tumor necrosis factor alpha (TNF-alpha), interleukin 6, and heat shock protein 90 (Hsp90) contents were reduced in TFPPL-treated mice. In histopathological observations, TFPPL-treated mice exhibited reduced hepatocellular Hsp90, TNF-alpha, nuclear factor kappa-light-chain-enhancer of activated B cells-p65 positive cells, and lowered Bax and caspase-3-labeled cells in the livers. Further, intrasplenic integrin beta 1, 5 '-nucleotidase, and antigen KI-67 positive cells were increased after TFPPL treatments. Taken together, our present findings demonstrate that herb-extracted TFPPL exert potential hepatoprotective activities against chemical-induced liver damage in mice, possibly through the pharmacological mechanisms of inhibiting inflammatory stress and apoptosis, inactivating Hsp90 bioactivity in the liver, and improving splenic immunocompetence.
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