Efficient Preparation of Black Tea Extract (BTE) with the High Content of Theaflavin Mono- and Digallates and the Protective Effects of BTE on CCl4-Induced Rat Liver and Renal Injury.
Jianfeng ZhanHoujian CaoTing HuJunfeng ShenWeixin WangPeng WuGuliang YangChi-Tang HoShiming LiPublished in: Journal of agricultural and food chemistry (2021)
Theaflavins (TFs), formed by the dimerization of green tea catechins during "fermentation" to prepare black tea, possess antioxidant and anti-inflammatory effects. Reported efficacious effects of black tea (∼2% of TFs) or related products come from catechins unless TFs are assayed. The present study aimed to target the preparation of black tea extract (BTE) enriched with theaflavin mono- and digallates majorly from dry tea leaves in aqueous media versus traditional fermentation of fresh leaves. We further investigated the protective function of the produced BTE on rat liver and kidney injury induced by CCl4 and its underlying molecular mechanisms. The results showed that BTE suppressed the activation level of hepatic stellate cells (HSCs), and the secretion of collagen was induced by CCl4. The relative expression levels of TGF-β, p-ERK1/ERK1, p-ERK2/ERK2, p-Smad1/Smad1, and p-Smad2/Smad2 were reduced to 56, 68, 56, 44, and 32%, respectively, compared with those of CCl4-treated rats. Therefore, BTE enriched with TFs prevented rat hepatic fibrosis through the TGF-β/Smad/ERK signaling pathway and kidney injury by inhibiting the expression of TGF-β and proinflammatory cytokines in rats. We predict the broad application of TFs and related products because of their strong antioxidant and inhibitory effects on chronic inflammation.
Keyphrases
- signaling pathway
- transforming growth factor
- epithelial mesenchymal transition
- oxidative stress
- induced apoptosis
- pi k akt
- liver fibrosis
- liver injury
- drug induced
- cell cycle arrest
- diabetic rats
- poor prognosis
- anti inflammatory
- cell proliferation
- binding protein
- saccharomyces cerevisiae
- long non coding rna
- lactic acid
- mass spectrometry
- endoplasmic reticulum stress