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Betulinic acid prevents alcohol-induced liver damage by improving the antioxidant system in mice
Jine Yi,Wei Xia,Jianping Wu,Li-yun Yuan,Jing Wu,Di Tu,Jun Fang,Zhuliang Tan 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.1
Betulinic acid (BA), a pentacyclic lupane-type triterpene, hasa wide range of bioactivities. The main objective of this workwas to evaluate the hepatoprotective activity of BA and thepotential mechanism underlying the ability of this compoundto prevent liver damage induced by alcohol in vivo. Mice weregiven oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14days, and induced liver injury by feeding 50% alcohol orally atthe dosage of 10 ml/kg after 1 h last administration of BA. BApretreatment significantly reduced the serum levels of alaninetransaminase, aspartate transaminase, total cholesterol, andtriacylglycerides in a dose-dependent manner in the miceadministered alcohol. Hepatic levels of glutathione, superoxidedismutase, glutathione peroxidase, and catalase wereremarkably increased, while malondialdehyde contents andmicrovesicular steatosis in the liver were decreased by BA in adose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying thehepatoprotective effects of BA might be due to increasedantioxidant capacity, mainly through improvement of thetissue redox system, maintenance of the antioxidant system,and decreased lipid peroxidation in the liver.
Sijun Deng,Hui Yuan,Jine Yi,Yin Lu,Qiang Wei,Chengzhi Guo,Jing Wu,Zuping He,Li-yun Yuan 대한수의학회 2013 Journal of Veterinary Science Vol.14 No.3
To investigate the effects of gossypol acetic acid (GA) on proliferation and apoptosis of the macrophage cell line RAW264.7 and further understand the possible underlying mechanism responsible for GA-induced cell apoptosis,RAW264.7 cells were treated with GA (25∼35 μmol/L) for 24h and the cytotoxicity was determined by MTT assay, while apoptotic cells were identified by TUNEL assay, acridine orange/ethidium bromide staining and flow cytometry. Moreover, mitochondrial membrane potential (ΔΨ m) with Rhodamine 123 and reactive oxygen species (ROS) with DCFH-DA were analyzed by fluorescence spectrofluorometry. In addition, the expression of caspase-3 and caspase-9 was assessed by Western Blot assay. Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK,respectively. GA significantly inhibited the proliferation of RAW264.7 cells in a dose-dependent manner, and caused obvious cell apoptosis and a loss of ΔΨ m in RAW264.7 cells. Moreover, the ROS production in cells was elevated, and the levels of activated caspase-3 and caspase-9 were up-regulated in a dose-dependent manner. Notably, GA-induced cell apoptosis was markedly inhibited by caspase inhibitors. These results suggest that GA-induced RAW264.7 cell apoptosis may be mediated via a caspase-dependent mitochondrial signaling pathway.
Angelica dahurica attenuates melanogenesis in B16F0 cells by repressing Wnt/β-catenin signaling
Fang Chien-Liang,Goswami Debakshee,Kuo Chia-Hua,Day Cecilia Hsuan,Lin Mei-Yi,Ho Tsung-Jung,Yang Liang-Yo,Hsieh Dennis Jine-Yuan,Lin Tzu-Kai,Huang Chih-Yang 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.1
Background Melanogenesis is a complex process which is tightly regulated by several enzymes. However, abnormal melanogenesis can cause severe dermatological problems. Roots of Angelica dahurica have been used for skin care as a part of traditional Chinese medicine for many generations. However, the role of A. dahurica in melanogenesis remains unclear. Objective Previous in vitro and in vivo studies have demonstrated that NK-1R exerts positive effects in melanogenesis via the Wnt/βcatenin signaling pathway. In this study, we investigated the effects of A. dahurica ethanol extract (ADE) on NK-1R and Wnt/β-catenin signaling, and evaluated the effect of NK-1R on melanogenesis in B16F0 cells. Results Angelica dahurica ethanol extract efficiently downregulated Neurokinin-1 receptor and Wnt/β-catenin signaling by decreasing the expression of β-catenin, MITF, LEF-1, TYR, TRP1, and TRP2 and increasing the expression of GSK3β, which resulted from the weakened expression of the Neurokinin-1 receptor inhibitor [Sar9,Met(O2 )11]-Substance P (SMSP). Furthermore, the intracellular melanin assay and cellular tyrosinase activity confirmed these findings. Conclusion This study suggests that ADE has potential to downregulate Neurokinin-1 receptor in SMSP-induced B16F0 cells, thereby repressing the Wnt/β-catenin signaling and reduces melanin production.