• Title/Summary/Keyword: GPx

Search Result 450, Processing Time 0.039 seconds

Neuroprotective Effects of Stachys sieboldii Miq. Extract Against Ischemia/reperfusion-induced Apoptosis in SH-SY5Y Neuroblastoma Cells (허혈-재관류 유도 신경세포사멸에 대한 초석잠 추출물의 신경보호 효과 연구)

  • Young-Kyung Lee;Chul Hwan Kim;Su Young Shin;Buyng Su Hwang;Min-Jeong Seo;Hye Jin Hwang;Kyung-Min Choi;Jin-Woo Jeong
    • Proceedings of the Plant Resources Society of Korea Conference
    • /
    • 2020.08a
    • /
    • pp.76-76
    • /
    • 2020
  • Stachys sieboldii Miq. (chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of Stachys sieboldii Miq. (SSM) in cerebral ischemia/reperfusion (I/R) injury is not yet fully understood. In the current study, the neuroblastoma cell line (SH-SY5Y) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to simulate I/R injury in vitro model. The results showed that SSM improved OGD/R-induced inhibitory effect on cell viability of SH-SY5Y Cells. SSM displayed anti-oxidative activity as proved by the decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in OGD/R-induced SH-SY5Y Cells. In addition, cell apoptosis was markedly decreased after SSM treatment in OGD/R-induced SH-SY5Y Cells. The up-regulation of Bcl-2 and down-regulation of Bax, thus reducing the Bax/Bcl-2 ratio that in turn protected the activation of caspase-9 and -3, and inhibition of poly (ADP-ribose) polymerase cleavage, which was associated with the blocking of cytochrome c release to the cytoplasm. Collectively, SSM protected human neuroblastoma SH-SY5Y cells from OGD/R-induced injury via preventing mitochondrial-dependent pathway through scavenging excessive ROS, suggesting that SSM might be a potential agent for the ischemic stroke therapy.

  • PDF

Stachys sieboldii M iq. Protects SH-SY5Y Cells Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury by Inhibition of Mitochondrion-Mediated Apoptosis Pathway (허혈-재관류 유도 SH-SY5Y 모델에서 미토콘드리아 매개 Apoptosis 기전 제어를 통한 초석잠 추출물의 세포보호 효과)

  • Jin-Woo Jeong;Eun Jung Ahn;Chul Hwan Kim;Su Young Shin;Seung Young Lee;Kyung-Min Choi;Chang-Min Lee
    • Proceedings of the Plant Resources Society of Korea Conference
    • /
    • 2021.04a
    • /
    • pp.57-57
    • /
    • 2021
  • Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. Stachys sieboldii Miq. (Chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of S. sieboldii Miq. (SSM) in OGD/R induced neuronal injury is not yet fully understood. The present research is aimed to investigate the protective effect and possible mechanisms of SSM extract treatment in an in vitro model of OGD/R to simulate ischemia/reperfusion Injury. Pretreatment of these cells with SSM significantly attenuated OGD/R-induced production of reactive oxygen species (ROS) by increasing GPx, SOD, and decreasing MDA. SSM decreased mitochondrial damage caused by OGD/R injury and inhibited the release of cyt-c from mitochondrion to cytoplasm in SH-SY5Y cells. Furthermore, neuronal cell apoptosis caused by OGD/R injury was inhibited by SSM, and SSM could decrease apoptosis by increasing ratio of Bcl-2/Bax and inhibiting caspase signaling pathway in SH-SY5Y cells. SSM demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro model, and this effect was the inhibition of mitochondria-mediated apoptosis pathway by scavenging of ROS generation. Therefore, SSM may be a promising neuroprotective strategy against ischemic stroke.

  • PDF

LncRNA AC005332.7 Inhibited Ferroptosis to Alleviate Acute Myocardial Infarction Through Regulating miR-331-3p/CCND2 Axis

  • Rixin Dai;Xiheng Yang;Wujin He;Qiang Su;Xuexin Deng;Juanfen Li
    • Korean Circulation Journal
    • /
    • v.53 no.3
    • /
    • pp.151-167
    • /
    • 2023
  • Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions: AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.

Protective effect of Phyllostachys edulis (Carrière) J. Houz against chronic ethanol-induced cognitive impairment in vivo

  • Jiyeon Kim;Ji Myung Choi;Ji-Hyun Kim;Qi Qi Pang;Jung Min Oh;Ji Hyun Kim;Hyun Young Kim;Eun Ju Cho
    • Nutrition Research and Practice
    • /
    • v.18 no.4
    • /
    • pp.464-478
    • /
    • 2024
  • BACKGROUND/OBJECTIVES: Chronic alcohol consumption causes oxidative stress in the body, which may accumulate excessively and cause a decline in memory; problem-solving, learning, and exercise abilities; and permanent damage to brain structure and function. Consequently, chronic alcohol consumption can cause alcohol-related diseases. MATERIALS/METHODS: In this study, the protective effects of Phyllostachys edulis (Carrière) J. Houz (PE) against alcohol-induced neuroinflammation and cognitive impairment were evaluated using a mouse model. Alcohol (16%, 5 g/kg/day for 6 weeks) and PE (100, 250, and 500 mg/kg/day for 21 days) were administered intragastrically to mice. RESULTS: PE showed a protective effect against memory deficits and cognitive dysfunction caused by alcohol consumption, confirmed through behavioral tests such as the T-maze, object recognition, and Morris water maze tests. Additionally, PE attenuated oxidative stress by reducing lipid oxidation, nitric oxide, and reactive oxygen species levels in the mice's brains, livers, and kidneys. Improvement of neurotrophic factors and downregulation of apoptosis-related proteins were confirmed in the brains of mice fed low and medium concentrations of PE. Additionally, expression of antioxidant enzyme-related proteins GPx-1 and SOD-1 was enhanced in the liver of PE-treated mice, related to their inhibitory effect on oxidative stress. CONCLUSION: This suggests that PE has both neuroregenerative and antioxidant effects. Collectively, these behavioral and histological results confirmed that PE could improve alcohol-induced cognitive deficits through brain neurotrophic and apoptosis protection and modulation of oxidative stress.

Neuroprotective effects of cultured and fermented wild ginseng extracts on oxidative stress induced by hydrogen peroxide in PC12 cells (발효산삼배양근농축액의 산화방지 효과 및 과산화수소로 유발된 PC12 세포독성 보호효과)

  • Choi, Yeo Ok;Kim, Yu-Ri;Shin, Seung-Yong;Lee, Jae Geun;Kim, Chul Joong;Lee, Ye ji;Kang, Byeongju;Kim, Gwansu;Choi, Jee Eun;Han, Beom-Seok
    • Korean Journal of Food Science and Technology
    • /
    • v.50 no.4
    • /
    • pp.383-390
    • /
    • 2018
  • Most neurodegenerative diseases are known to be influenced by oxidative stress. We investigated the anti-oxidative activity of the concentrate of fermented wild ginseng root culture (HLJG0701) containing ginsenosides Rg5 and Rk1. HLJG0701 showed effective DPPH and ABTS radical scavenging ability ($IC_{50}$: 16- and 4-fold dilution, respectively) and was inhibited dose-dependently by the $FeSO_4$-induced lipid peroxidation group (8- and 4-fold dilution: 2.3 and 1.5 nM, respectively). In MTT and LDH assays, 8-, 16-, 32- and 64-fold diluted HLJG0701 significantly increased cell viability by 70, 53, 35, and 26%, respectively. LDH released by HLJG0701 was reduced 1.3-fold with 8-fold diluted HLJG0701 compared to the $H_2O_2$-treated control. In addition, the inhibitory effect of HLJG0701 on oxidative stress in PC12 cells was confirmed by DCF-DA analysis (16-, 4-fold diluted HLJG0701: 50 and 68% ROS inhibition, respectively), TBARS (16- and 4-fold diluted HLJG0701: 50.7 and 46.5% inhibition, respectively), GPx (16- and 4-fold diluted HLJG0701: 133.3 and 227.3% release, respectively), and SOD analysis (16- and 4-fold diluted HLJG0701: 118.2 and 218.2% release, respectively). These results suggested that HLJG0701 protects neuronal cells by its anti-oxidative effects and hence can be a potential preventive material against neurodegenerative diseases.

Antioxidant Activities and Hepato-protective Effects of Stauntonia hexaphylla Fruit Extract Against H2O2-induced Oxidative Stress and Acetaminophen-induced Toxicity (멀꿀 열매 추출물의 항산화 활성 및 H2O2로 유도된 산화적 스트레스와 아세트아미노펜 독성 모델에서의 간 보호효과)

  • Lee, Gyuok;Kim, Jaeyong;Kang, Huwan;Bae, Donghyuck;Choi, Chul-yung
    • Journal of Life Science
    • /
    • v.28 no.6
    • /
    • pp.708-717
    • /
    • 2018
  • The antioxidant activity and protective effects of a hot water extract from the Stauntonia hexaphylla fruit (WESHF) were investigated in vitro and in vivo. The total polyphenol and flavonoid contents of WESHF were $16.13{\pm}0.27mg$ gallic acid equivalent/g and $4.7{\pm}0.80mg$ catechin equivalent/g, respectively. In addition, the DPPH radical-scavenging activity ($SC_{50}$) and the Oxygen Radical Absorbance capacity of WESHF were $63.62{\pm}4.10{\mu}g/ml$ and $90.63{\pm}5.29{\mu}M$ trolox equivalent/g, respectively. The hepatoprotective effect of WESHF against hydrogen peroxide-induced oxidative damage was investigated. $H_2O_2$-induced liver damage on HepG2 cells was prevented by $200{\mu}g/ml$ of WESHF. Furthermore, to investigate the protection mechanism of WESHF on hydrogen peroxide-induced cytotoxicity in HepG2 cells, pre-treatment with $200{\mu}g/ml$ of WESHF significantly attenuated a decrease in the activities of CAT, SOD, GR, and GPx. The hepatoprotective activity of WESHF was evaluated in an experimental model of hepatic damage induced by acetaminophen (APAP). The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly decreased in the livers of mice treated with 200 mg/kg of WESHF compared to the APAP-treated group. The lipid peroxidation level, which increased after APAP administration, was significantly reduced in the WESHF group. In addition, histological examinations of the liver showed the same protective effect of WESHF treatment. Based on these findings, it is suggested that WESHF has potent hepatoprotective effects, and the mechanism that causes this type of protection could be related to antioxidant pathways.

Dietary Effects of Fermented Soybean Curd Residue (Biji) on Body Weight, Serum Lipid Profiles, and Antioxidation-Related Enzymes Activity of Mice Fed a High Fat Diet (고지방식이 마우스의 체중과 혈청지질 및 항산화계 효소활성에 미치는 발효 비지의 식이효과)

  • Lee, Sang-Il;Lee, Ye-Kyung;Kim, Soon-Dong;Lee, In-Ae;Choi, Jongkeun;Suh, Joo-Won
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.42 no.7
    • /
    • pp.1043-1053
    • /
    • 2013
  • We investigated the ability of soybean curd residue (SCR) and its fermented products to inhibit obesity and improve the blood lipid profiles of obese mice fed a high-fat diet. Samples were prepared by fermenting SCR with Aspergillus oryzae var effuses KACC 44990 (ASCR), a microbe used for the fermentation of traditional Korean Meju, and with Monascus pilosus IFO 4480 (MSCR), a microbe used for the production of red rice. In addition, AMSCR, a mixture composed of equal amounts of ASCR and MSCR, was also prepared. Male mice were divided into six groups and fed with either a normal diet, a high-fat diet, or a high-fat diet supplemented with SCR, ASCR, MSCR, or AMSCR. After 8 weeks, body weight gain, serum and hepatic lipid profiles, and the activities of enzymes that generate or scavenge reactive oxygen species (ROS) were evaluated. Compared with the high-fat diet group, all the test groups showed a significant reduction in body, organ, and epididymal fat weight gain. These effects were observed with supplements in the order AMSCR>ASCR>MSCR>SCR. Similarly, supplements of test samples reduced high levels of serum and hepatic triglycerides (TG), total cholesterol, and low-density lipoprotein (LDL) cholesterol caused by hight-fat diet, while high-density lipoprotein (HDL) cholesterol was increased. Interestingly, the ability of ASCR to lower serum TG was stronger than that of MSCR, while MSCR showed a stronger hypocholesterolemic effect than ASCR. Meanwhile, AMSCR returned comprehensively serum lipid levels to normal. In addition, hepatic damage was prevented with effects in the order AMSCR>ASCR>MSCR>SCR. Hepatic ROS generating system including xanthine oxidase (XO) and ROS scavenging system including superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione S-transferase (GST) were recovered to normal level by all test diets. In conclusion, this study suggests that SCR and its fermented products can inhibit obesity and improve lipid profiles.

Protective Effects of Radiation-induced Blackberry Mutant Extract on Carbon Tetrachloride (CCl4)-induced Liver Injury in Sprague-Dawley Rats (방사선 돌연변이 블랙베리 추출물의 사염화탄소(Carbon Tetrachloride, CCl4) 투여에 의한 흰쥐의 간 손상에 대한 보호 효과)

  • Cho, Byoung Ok;Lee, Chang-Wook;So, Yangkang;Jin, Chang-Hyun;Yook, Hong-Sun;Byun, Myung-Woo;Jeong, Yong-Wook;Park, Jong Chun;Jeong, Il-Yun
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.43 no.6
    • /
    • pp.807-813
    • /
    • 2014
  • The objective of the present study was to investigate the protective effects of anthocyanin-enriched extract from radiation-induced blackberry (Rubus fruticosus L.) mutant (${\gamma}$-B201) against carbon tetrachloride ($CCl_4$)-induced liver injury in Spargue-Dawley (SD) rats. The in vivo results show that ${\gamma}$-B201 attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in $CCl_4$-treated SD rats. Histopathological examination of rat livers showed that ${\gamma}$-B201 reduced the incidence of liver lesions induced by $CCl_4$. Moreover, ${\gamma}$-B201 prevented DNA damage in $CCl_4$-treated SD rats. Furthermore, administration of ${\gamma}$-B201 significantly increased the activity of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), in $CCl_4$-treated rat livers. In conclusion, the present study suggests that ${\gamma}$-B201 blackberry extract protects the liver from $CCl_4$-induced hepatic damage through an antioxidant mechanism. Therefore, ${\gamma}$-B201 blackberry may be functional food material for human health.

Effects of Turmeric (Curcuma longa L.) on Antioxidative Systems and Oxidative Damage in Rats Fed a High Fat and Cholesterol Diet (울금(Curcuma longa L.)이 고지방·고콜레스테롤 식이 흰쥐의 항산화계 및 산화적 손상에 미치는 영향)

  • Kim, Min-Sun;Chun, Sung-Sik;Choi, Jeong-Hwa
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.42 no.4
    • /
    • pp.570-576
    • /
    • 2013
  • The purpose of this study was to investigate the effect of turmeric on antioxidative systems and oxidative damage in rats fed a high fat and cholesterol diet. A total 40 rats were divided into four experimental groups: a normal diet group (N), a high fat and cholesterol diet group (HF), a high fat and cholesterol diet group supplemented with 2.5% turmeric powder (TPA group) and a high fat and cholesterol diet group supplemented with 5% turmeric powder (TPB group). The serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) activity of the turmeric supplemented groups were decreased compared to the HF group. The GPT activity of the TPB group was especially and significantly decreased compared to the HF group. Hepatic superoxide dismutase (SOD) of the TPB group was significantly increased compared to the HF group. However, there were no significant differences in the activities of hepatic glutathione peroxidase (GSHpx) and catalase (CAT) among all experimental groups. Hepatic glutathione S-transferase (GST) activity in the TPA and TPB groups were increased compared to the HF group. Hepatic superoxide radical content in mitochondria of the 5% turmeric supplemented group was significantly decreased compared to the HF group. Hepatic hydrogen peroxide content in the cytosol and mitochondria of the turmeric-supplemented groups were decreased compared to the HF group. Hepatic carbonyl values in the mitochondria of the turmeric supplemented groups were significantly decreased compared to the HF group. Thiobarbituric acid reaction substance (TBARS) values in the liver were significantly reduced in turmeric supplemented groups compared to the HF group. These result suggest that turmeric powder may reduce oxidative damage through the activation of antioxidative defense systems in rats fed high fat and cholesterol diets.

The Effect of protein and lipioperoxide on White Ginseng(WG) and Fermenta Ginseng(FG) Extracts on the liver in Mice that was irradiated by radiation (방사선이 조사된 생쥐 간에서 백삼과 발효인삼추출물이 단백질 및 지질과산화에 미치는 효과)

  • Ko, In-Ho;Chang, Chae-Chul;Koh, Jeong-Sam
    • Journal of radiological science and technology
    • /
    • v.27 no.3
    • /
    • pp.43-50
    • /
    • 2004
  • The effects of ginseng extracts on liver damage induced by high energy x-ray were studied. To one group of ICR male mice were given white(50 mg/kg/day for 7 days, orally) and fermenta ginseng extracts(500 mg/kg/day for 7 days, orally)before irrdiation. To another group were irradiated by 5 Gy dose of high energy x-ray. Contrast group were given with saline(0.1 ml). This study also investigated the effect between MDA, protein content and ginseng extracts on hepatic damage. This study measured the level of MDA(malondialdehyde), protein content in liver tissue. Administrating orally white (50 mg/kg/day for 7 days, orally)and fermenta ginseng extracts(500 mg/kg/day), the level of MDA were generally decreased and the inhibition was increased. And the protein contents were identical with control group. After irradiation, the protein contents were increased and MDA(malondialdehyde) was increased. Therefore, ginseng extracts increased antioxidative enzyme activity. And We know that the antioxidatant effect of extracts from white and fermenta ginseng protect radiation damage by direct antioxidant effect involving SOD, CAT, GPX. It was included that ginsengs can protect against the lipid peroxidation in radiation damage through its antioxidatant properties.

  • PDF