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Published on: September 15, 2017
Exploring the potential active components and mechanisms of Tetrastigma hemsleyanum against ulcerative colitis based
Qiang Zhang1, Tinghui Feng2, Qinxiang Chang1
1College of Life Sciences, Key Laboratory of Plant Secondary Metabolism and Regulation of Zhejiang Province, Zhejiang Sci-Tech University, Xuelin Road, Xiasha District, Hangzhou, 310018, People's Republic of China.
Ethnopharmacological Relevance:
Ulcerative colitis (UC) is a chronic form of inflammatory bowel disease, which current treatments often show limited effectiveness. Ferroptosis, a newly recognized form of programmed cell death has been implicated in UC pathogenesis, suggesting that it may be viable therapeutic target. Tetrastigma hemsleyanum (TH) has shown potential anti-UC effects, though it is unclear whether its therapeutic benefits are mediated by ferroptosis.
Aim Of The Study:
This study investigated the involvement of ferroptosis in the therapeutic effects of TH and identified key active components and pathways of TH against UC.
Materials And Methods:
The ethyl acetate extract of TH (TH_E) was found to be the most effective anti-inflammatory extract compared with the petroleum ether extract (TH_P), n-butanol extract (TH_N), and water-soluble extract (TH_W). TH_E's components were identified using UHPLC-MS/MS, ADME parameters, and network pharmacology. Additionally, TH_E's effects on ferroptosis were evaluated in an LPS-induced RAW264.7 cell model.
Results:
TH_E exhibited the strongest anti-inflammatory activity among four extracts. 10 compounds (Linolenic acid; Apigenin; Protocatechualdehyde; Asiatic acid; Quercetin; Isorhamnetin; Kaempferol; Azelaic acid; Oleic Acid; Palmitic acid) were selected from SwissADME database. Then a total of 281 targets for these 10 compounds and 1330 UC-related targets were identified from different database. Isorhamnetin was selected as the most promising anti-inflammatory component among 10 components. Furthermore, enrichment analysis revealed that ferroptosis was involved in UC development, with both TH_E and isorhamnetin exhibited inhibition of ferroptosis. Finally, isorhamnetin's anti-ferroptosis effects were linked to the Keap1/Nrf2/HO-1 pathway.
Conclusions:
The results demonstrate that TH_E and isorhamnetin alleviate LPS-induced UC through restraining ferroptosis. Moreover, isorhamnetin's anti-UC properties are mediated by inhibiting ferroptosis via activation of the Keap1/Nrf2/HO-1 axis.
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