Ethyl acetate extract of Wedelia chinensis inhibits tert-butyl hydroperoxide-induced damage in PC12 cells and D-galactose-induced neuronal cell loss in mice

Lin, Wea‐Lung; Wang, Shao-Ming; Ho, Ying-Jui; Kuo, Hsing‐Chun; Lee, Yean‐Jang; Tseng, Tsui‐Hwa

doi:10.1186/1472-6882-14-491

Cited by 11 publications

(8 citation statements)

References 29 publications

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“…ROS are predominantly produced in mitochondria. It has been reported that the mitochondria-dependent apoptotic pathway is involved in t -BHP-induced cytotoxicity, in which the Bcl-2 family proteins play a key role [ 24 ]. The anti-apoptotic Bcl-2 bind to the outer membrane of the mitochondria can stabilize the membrane permeability and prevent the release of cytochrome c [ 25 ], while the pro-apoptotic members like Bax are responsible for permeabilizing membrane under cellular stress [ 26 , 27 ].…”

Section: Resultsmentioning

confidence: 99%

Antioxidant and Hepatoprotective Effect of Penthorum chinense Pursh Extract against t-BHP-Induced Liver Damage in L02 Cells

Wang

et al. 2015

Molecules

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Penthorum chinense Pursh (P. chinense), a traditional Chinese medicine used by the Chinese Miao minority, has been used to treat liver diseases for a long time. However, the mechanism behind the liver protective effects of P. chinense remains unclear so far. The aim of the present study was to investigate the hepatoprotective effect of P. chinense and its possible mechanism(s). Immortalized normal human normal liver L02 cells were used to evaluate the protective effect of P. chinense aqueous extract against tert-butyl hydroperoxide (t-BHP)-induced liver cell damage. Treatment with P. chinense aqueous extract significantly protected L02 cells from t-BHP-induced cytotoxicity, prevented t-BHP-induced reactive oxygen species (ROS) generation and decreased the percentage of apoptosis by inhibiting the mitochondrial apoptotic pathway. This study demonstrates that P. chinense is a potential hepatoprotective agent in t-BHP-induced liver cell damage, which may benefit the further application of P. chinense in the clinic.

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Section: Resultsmentioning

confidence: 99%

Antioxidant and Hepatoprotective Effect of Penthorum chinense Pursh Extract against t-BHP-Induced Liver Damage in L02 Cells

Wang

et al. 2015

Molecules

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“…We observed in the present study that treatment with 300 mM Dg for 48 h induced cellular senescence in SY5Y cells. Previously, it was reported that Dg treatment efficiently induced senescence not only in animal models, but also in in vitro cell models [ 12 33 34 ]. For example, Wang et al [ 35 ] and Rahimi et al [ 36 ] reported that 200–400 mM Dg could cause senescence in RA-induced differentiated SY5Y cells as a result of increased oxidative stress and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Curcumin and hesperetin attenuate D-galactose-induced brain senescencein vitroandin vivo

Lee

Kim

et al. 2020

Nutr Res Pract

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BACKGROUND/OBJECTIVES: Brain senescence causes cognitive impairment and neurodegeneration. It has also been demonstrated that curcumin (Cur) and hesperetin (Hes), both antioxidant polyphenolic compounds, mediate anti-aging and neuroprotective effects. Therefore, the objective of this study was to investigate whether Cur, Hes, and/or their combination exert anti-aging effects in D-galactose (Dg)-induced aged neuronal cells and rats. MATERIALS/METHODS: SH-SY5Y cells differentiated in response to retinoic acid were treated with Cur (1 μM), Hes (1 μM), or a combination of both, followed by 300 mM Dg. Neuronal loss was subsequently evaluated by measuring average neurite length and analyzing expression of β-tubulin III, phosphorylated extracellular signal-regulated kinases, and neurofilament heavy polypeptide. Cellular senescence and related proteins, p16 and p21, were also investigated, including their regulation of antioxidant enzymes. In vivo, brain aging was induced by injecting 250 mg/kg body weight (b.w.) Dg. The effects of supplementing this model with 50 mg/kg b.w. Cur, 50 mg/kg b.w. Hes, or a combination of both for 3 months were subsequently evaluated. Brain aging was examined with a step-through passive avoidance test and apoptosis markers were analyzed in brain cortex tissues. RESULTS: Cur, Hes, and their combination improved neuron length and cellular senescence by decreasing the number of β-gal stained cells, down-regulated expression of p16 and p21, and up-regulated expression of antioxidant enzymes, including superoxide dismutase 1, glutathione peroxidase 1, and catalase. Administration of Cur, Hes, or their combination also tended to ameliorate cognitive impairment and suppress apoptosis in the cerebral cortex by downregulating Bax and poly (ADP-ribose) polymerase expression and increasing Bcl-2 expression. CONCLUSIONS: Cur and Hes appear to attenuate Dg-induced brain aging via regulation of antioxidant enzymes and apoptosis. These results suggest that Cur and Hes may mediate neuroprotective effects in the aging process, and further study of these antioxidant polyphenolic compounds is warranted.

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“…As a frequent event in nervous system, it is therefore associated with a wide range of neurological diseases (1,2). OS is an important therapeutic target, and the supplement of exogenous antioxidants has been validated to be an effective approach to prevent and manage neurological diseases clinically (13)(14)(15)(16). In the present study, neuronal SH-SY5Y cells underwent OS following exposure to H 2 O 2 , as indicated by TAC and MDA assays, and post-treatment with α-Naphthoflavone and/or β-Naphthoflavone effectively alleviated H 2 O 2 -induced OS.…”

Section: Discussionmentioning

confidence: 99%

α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage

Zhu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have demonstrated an association between neurological diseases and oxidative stress (OS).Naphthoflavone is a synthetic derivative of naturally occurring flavonoids that serves an important role in the treatment and prevention of OS-related diseases. The current study was designed to apply α-and β-Naphthoflavone individually and in combination to counteract the detrimental effects of OS on neurons in vitro. Neuronal SH-SY5Y cells were subjected to 20 µM H 2 O 2 , followed by exposure to 20 µM α-Naphthoflavone and/or 10 µM β-Naphthoflavone. Results indicated that α-and β-Naphthoflavone effectively antagonized the apoptosis-promoting effect of H 2 O 2 on neuronal SH-SY5Y cells, and that β-Naphthoflavone significantly (P<0.05) reversed H 2 O 2 -inhibited cell viability. Notably, co-treatment of α-and β-Naphthoflavone reversed the H 2 O 2 -induced apoptosis rate elevation and cell viability reduction. Further analysis demonstrated that H 2 O 2 inhibited the activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase, but this was reversed by the co-treatment with α-and β-Naphthoflavone and selectively enhanced by the treatment with α-or β-Naphthoflavone. H 2 O 2 -stimulated p38 mitogen-activated protein kinase activation was repressed following treatment with α-and/or β-Naphthoflavone, along with a decreased expression of the apoptosis-related factors and inhibited caspase-3 activation. In conclusion, co-treatment with α-and β-Naphthoflavone minimized H 2 O 2 -led neuron damage compared with treatment with α-or β-Naphthoflavone, suggesting a synergetic effect between α-and β-Naphthoflavone. This indicates that utilizing α-and β-Naphthoflavone together in the clinical setting may provide a novel therapeutic for neurological disease.

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Ethyl acetate extract of Wedelia chinensis inhibits tert-butyl hydroperoxide-induced damage in PC12 cells and D-galactose-induced neuronal cell loss in mice

Cited by 11 publications

References 29 publications

Antioxidant and Hepatoprotective Effect of Penthorum chinense Pursh Extract against t-BHP-Induced Liver Damage in L02 Cells

Antioxidant and Hepatoprotective Effect of Penthorum chinense Pursh Extract against t-BHP-Induced Liver Damage in L02 Cells

Curcumin and hesperetin attenuate D-galactose-induced brain senescencein vitroandin vivo

α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage

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