Protective Activity of Seolitae Chungkukjang Added with Green Tea against Cellular Oxidative Stress induced by AAPH

2009 ◽  
Vol 14 (1) ◽  
pp. 37-42
Author(s):  
Hyun-Young Park ◽  
Hee-Seob Lee ◽  
Eun-Ju Cho
2007 ◽  
Vol 12 (4) ◽  
pp. 191-196 ◽  
Author(s):  
Mi-Jung So ◽  
Boh-Kyung Kim ◽  
Mi-Jin Choi ◽  
Kun-Young Park ◽  
Sook-Hee Rhee ◽  
...  

2008 ◽  
Vol 4 (4) ◽  
pp. 365-370 ◽  
Author(s):  
S. Ounjaijean ◽  
C. Thephinlap ◽  
U. Khansuwan ◽  
C. Phisalapong ◽  
S. Fucharoen ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1076
Author(s):  
Guoyi Tang ◽  
Yu Xu ◽  
Cheng Zhang ◽  
Ning Wang ◽  
Huabin Li ◽  
...  

Nonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.


2005 ◽  
Vol 27 (9) ◽  
pp. 655-660 ◽  
Author(s):  
Dong-Wook Han ◽  
Hak Hee Kim ◽  
Mi Hee Lee ◽  
Hyun Sook Baek ◽  
Kwon-Yong Lee ◽  
...  

2014 ◽  
Vol 57 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Alena Moravcová ◽  
Zuzana Červinková ◽  
Otto Kučera ◽  
Vojtěch Mezera ◽  
Halka Lotková

Literature data support that green tea and its major component epigallocatechin gallate (EGCG) have powerful antioxidant effects. Contrary, hepatotoxicity can be induced by high-dose EGCG. The timing of exposure to green tea in relation to administration of hepatotoxic agent plays an import role too. The aim of our work was a verification of antioxidative effect of EGCG on D-galactosamine-induced injury in primary culture of rat hepatocytes. Hepatocytes were incubated with EGCG at concentrations of 1.25–10 μM and toxic D-galactosamine (GalN) for 24 hrs. Alternatively, hepatocytes were pretreated with EGCG for 24 hrs, and then incubated with EGCG and GalN for further 24 hrs. Cytotoxicity was analysed by lactate dehydrogenase activity, functional capacity by albumin production. Oxidative stress was evaluated from a production of malondialdehyde and glutathione content in the cells. EGCG protected hepatocytes against GalN-induced cytotoxicity but preventive treatment of intact hepatocytes with EGCG was required to diminish the development of hepatocyte injury. Oxidative stress induced in our study seems to overcome the ability of hepatocytes to improve GSH depletion and albumin production. Prolongation of the pretreatment with EGCG could be a promising strategy leading to amelioration of its hepatoprotective effect.


2014 ◽  
Vol 25 (2) ◽  
pp. 126-135 ◽  
Author(s):  
Bradley J. Newsome ◽  
Michael C. Petriello ◽  
Sung Gu Han ◽  
Margaret O. Murphy ◽  
Katryn E. Eske ◽  
...  

2012 ◽  
Vol 22 (6) ◽  
pp. 486-496 ◽  
Author(s):  
Ewa Jówko ◽  
Jaroslaw Sacharuk ◽  
Bozena Balasinska ◽  
Jacek Wilczak ◽  
Malgorzata Charmas ◽  
...  

Purpose:To evaluate the effect of acute ingestion of green tea polyphenols (GTP) on blood markers of oxidative stress and muscle damage in soccer players exposed to intense exercise.Methods:This randomized, double-blinded study was conducted on 16 players during a general preparation period, when all athletes participated in a strength-training program focused on the development of strength endurance. After ingestion of a single dose of GTP (640 mg) or placebo, all athletes performed an intense muscle-endurance test consisting of 3 sets of 2 strength exercises (bench press, back squat) performed to exhaustion, with a load at 60% 1-repetition maximum and 1-min rests between sets. Blood samples were collected preexercise, 5 min after the muscle-endurance test, and after 24 hr of recovery. Blood plasma was analyzed for the concentrations of thiobarbituric acid–reacting substances (TBARS), uric acid (UA), total catechins, total antioxidant status (TAS), and activity of creatine kinase (CK); at the same time, erythrocytes were assayed for the activity of superoxide dismutase (SOD).Results:In both groups, plasma TBARS, UA, and TAS increased significantly postexercise and remained elevated after a 24-hr recovery period. SOD activity in erythrocytes did not change significantly in response to the muscle-endurance test, whereas in both groups plasma CK activity increased significantly after 24 hr of recovery. Acute intake of GTP cased a slight but significant increase in total plasma catechins. However, GTP was found not to exert a significant effect on measured parameters.Conclusions:Acute ingestion of GTP (640 mg) does not attenuate exercise-induced oxidative stress and muscle damage.


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