6-hydroxyluteolin 5,6,7,3',4'-pentamethyl ether/3',4',5,6,7-PENTAMETHOXYFLAVONE/Sinensetin/4H-1-Benzopyran-4-one, 2-(3,4-dimethoxyphenyl)-5,6,7-trimethoxy-/5,6,7,3',4'-pentamethoxyflavanone/2-(3,4-Dimethoxyphenyl)-5,6,7-trimethoxy-4H-chromen-4-one/Pedalitin permethyl ether/5,6,7,3',4'-Pentamethoxyflavone/2-(3,4-Dimethoxyphenyl)-5,6,7-trimethoxy-4H-1-benzopyran-4-one/Sinenstein
Methanol; Acetontrile; DMSO; DMF
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The present study was carried out to explore the effect of sinensetin in human T-cell lymphoma Jurkat cells and to reveal the underlying molecular mechanisms. We found that sinensetin significantly impeded Jurkat cell proliferation in a dose-dependent and time-dependent manner. Additionally, sinensetin treatment triggered apoptosis and autophagy in Jurkat cells. The apoptosis induction was related to a loss of mitochondrial membrane potential and to increased caspase-3/-8/-9 and poly(ADP-ribose) polymerase (PARP) cleavage. Sinensetin also induced autophagy, as evidenced by the formation of acidic vacuoles, the upregulation of LC3-II and beclin-1, and the downregulation of p62. In addition, the inhibition of autophagy by 3-methyladenine significantly enhanced the apoptosis rate and improved the sensitivity of the Jurkat cells to sinensetin. Moreover, sinensetin induced cell death, apoptosis, and autophagy through the activation of the reactive oxygen species/ c-Jun N-terminal kinase signaling pathway and the inhibition of the Akt/mTOR signaling pathways. In summary, our results revealed that sinensetin induced apoptosis and autophagy in human T-cell lymphoma Jurkat cells by activating reactive oxygen species/ c-Jun N-terminal kinase and blocking the Akt/mTOR signaling pathways. Thus, sinensetin might be a potential candidate in the development of antitumor drugs targeting T-cell leukemia.
Sinensetin Induces Apoptosis and Autophagy in the Treatment of Human T-cell Lymphoma
Kok-Tong Tan 1 2 , Meng-Xian Lin 1 , Shih-Chao Lin 3 , Yu-Tang Tung 4 , Sheng-Hao Lin 5 , Chi-Chien Lin 2 6
Sinensetin is a rare polymethoxylated flavone (PMF) found in certain citrus fruits. In this study, we investigated the effects of sinensetin on lipid metabolism in 3T3-L1 cells. Sinensetin promoted adipogenesis in 3T3-L1 preadipocytes growing in incomplete differentiation medium, which did not contain 3-isobutyl-1-methylxanthine. Sinensetin up-regulated expression of the adipogenic transcription factors peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein (C/EBP) α, and sterol regulatory element-binding protein 1c. It also potentiated expression of C/EBPβ and activation of cAMP-responsive element-binding protein. Sinensetin enhanced activation of protein kinase A and increased intracellular cAMP levels in 3T3-L1 preadipocytes. In mature 3T3-L1 adipocytes, sinensetin stimulated lipolysis via a cAMP pathway. Taken together, these results suggest that sinensetin enhances adipogenesis and lipolysis by increasing cAMP levels in adipocytes.
Sinensetin Enhances Adipogenesis and Lipolysis by Increasing Cyclic Adenosine Monophosphate Levels in 3T3-L1 Adipocytes
Seong-Il Kang 1 , Hye-Sun Shin, Se-Jae Kim
Background: Sarcopenia, the decline of skeletal muscle tissue attributed to primary aging is a major concern in older adults. Flavonoids might have potential benefits by modulating the regulation of satellite cells, thus preventing muscle loss. Sinensetin (SIN), a citrus methylated flavone with anti-inflammatory and anti-proliferative activity, can enhance lipolysis. The objective of the present study was to investigate whether SIN might have sarcopenia-suppressing effect on satellite cells from thigh and calf muscle tissues of young and old rats.
Methods: Primary muscle cells were obtained from thigh and calf tissues of young and old group rats by dissection. Obtained satellite cells were incubated with indicated concentrations of SIN (50 and 100 μM) treated and untreated condition in differentiation medium. Morphological changes of cells were examined using a phase-contrast microscope. Protein expression levels of myoD and myogenin were analyzed by Western blot. Cells treated with or without SIN under differentiation condition were also immunocytochemically stained for myogenin and 4′,6-diamidino-2-phenylindole (DAPI).
Results: Morphologically, the differentiation extracted satellite cells was found to be more evident in SIN treated group of aged rat’s cells than that in SIN untreated group. Expression levels of myoD and myogenin proteins involved in myogenesis were increased upon treatment with SIN.
Conclusions: Collectively, our results indicate that SIN can alleviate age-related sarcopenia by increasing differentiation rate and protein levels of myoD and myogenin.
MyoD; Myogenin; Sarcopenia; Sinensetin.
Sinensetin Regulates Age-Related Sarcopenia in Cultured Primary Thigh and Calf Muscle Cells
Jin-A Kim 1 , Seong Min Kim 2 , Sang Eun Ha 2 , Preethi Vetrivel 2 , Venu Venkatarame Gowda Saralamma 2 , Eun Hee Kim 3 , Gon Sup Kim 4
2019 Oct 28
Sinensetin is a methylated flavone found in certain citrus fruits. pocess potent antiangiogenesis and anti-inflammatory, sinensetin enhances adipogenesis and lipolysis.In vitro: Sinensetin promots adipogenesis in 3T3-L1 preadipocytes growing in incomplete differentiation medium, sinensetin enhances adipogenesis and lipolysis by increasing cAMP levels.  Sinensetin shows anti-inflammatory activity by regulating the protein level of inhibitor κB-α (IκB-α). In vivo: Sinensetin has the most potent antiangiogenesis activity and the lowest toxicity, inhibits angiogenesis by inducing cell cycle arrest in the G0/G1 phase in HUVEC culture and downregulating the mRNA expressions of angiogenesis genes flt1, kdrl, and hras in zebrafish.