scholarly journals Anti-oxidative and protective effect of soy tempeh on di(2-ethylhexyl)-phthalate (DEHP) injured FL83B mice liver cells

Author(s):  
Diana Lo ◽  
Reynetha DS Rawendra ◽  
Cian-Song Huang ◽  
Rupak Khatri-Chhetri ◽  
Yuh-Tai Wang ◽  
...  
Author(s):  
Fransisca Diana Alexandra ◽  
Dian Mutiasari ◽  
Trilianty Lestarisa ◽  
Eko Suhartono

The present study was undertaken to investigate the protective effect of ethanolic citronella grass (C. nardus) leaves extract against mercury (Hg) induced glucose metabolism alteration in rats. Four groups of rats were selected, with 6 rats for each group. Animals of group I was received a 1 ppm of Hg only. Animals of groups II, III, and IV received a combination of 1 ppm Hg and plant extract in different dose (1650, 2520, and 3360 mg/ml). The experiment lasted for 4 weeks. The various parameters studied included liver weight, liver glucose, glycogen, and malondialdehyde (MDA) level in all groups after treatment. The results of this present studies showed that the Hg-induced glucose metabolism alteration in rats which can be seen from the increase of liver glucose and the decreasing of liver glycogen levels. The results also showed that the Hginduced glucose metabolism alteration through its activities in the trigger the liver cells damage which can be seen from the decreasing of liver weight and the increase of liver MDA level. The ethanolic of C. nardus leaves extract shows a protective effect to maintain all parameters into a better a condition which can be seen from the significant increase in liver weight and liver glycogen level, and the significant decrease in liver glucose and MDA levels. The present study indicated that the ethanolic C. nardus leaves extract showed a potential protective effect on glucose metabolism alteration induced by Hg


2021 ◽  
Vol 784 ◽  
pp. 147221
Author(s):  
Hua-Jie Wang ◽  
Gang-Gang Yang ◽  
Sha-Sha Wu ◽  
Zhi-Fen Meng ◽  
Jia-Min Zhang ◽  
...  

2013 ◽  
Vol 70 (4) ◽  
pp. 560-565 ◽  
Author(s):  
Shigeru Suna ◽  
Masaaki Tokuda ◽  
Tomohiro Hirao ◽  
Fuminori Yamaguchi ◽  
Nobuyuki Miyatake ◽  
...  

1999 ◽  
pp. 35-39 ◽  
Author(s):  
M Gallo ◽  
M Aragno ◽  
V Gatto ◽  
E Tamagno ◽  
E Brignardello ◽  
...  

OBJECTIVE: Dehydroepiandrosterone (DHEA) is a widely studied steroid hormone with multi-functional properties. Reports suggest that some of the many activities of DHEA are due to its protective effect against lipid peroxidation. Nevertheless, the antioxidant properties of DHEA are still the subject of debate. The aim was to evaluate whether its two opposed effects on lipid peroxidation reported in the literature may be dependent on schedule and doses used. METHODS: Chang liver cells, a line derived from normal human liver, were grown in media containing either no steroids (control) or DHEA at concentrations ranging from 0.1 micromol/l to 50 micromol/l. At specific times, cultures were halted and cells received a pro-oxidant stimulus (cumene (CuOOH) 0.5 mmol/l), at which time cell viability (by trypan blue staining and lactate dehydrogenase (LDH) release) and thiobarbituric acid reactive substances (TBARS) concentration (spectrophotometrical assay) were evaluated. RESULTS: At concentrations ranging from 0.1 micromol/l to 1 micromol/l, DHEA protects Chang liver cells against lipid peroxidation and/or death induced by cumene. This effect disappears if the concentration is increased to 10 micromol/l; at higher concentrations (50 micromol/l) a pro-oxidant/cytotoxic effect of DHEA appears. CONCLUSIONS: DHEA exhibits two opposed effects on lipid peroxidation; depending on its concentration it acts either to limit or to induce oxidative stress. The threshold concentration at which the pro-oxidant activity of DHEA prevails is not far in excess of that having an antioxidant effect. Either effect of DHEA on lipid peroxidation is only evident after a 'lag-phase'.


2010 ◽  
Vol 49 (4) ◽  
pp. 559-566 ◽  
Author(s):  
Pınar Erkekoğlu ◽  
Walid Rachidi ◽  
Viviana De Rosa ◽  
Belma Giray ◽  
Alain Favier ◽  
...  

2015 ◽  
Vol 14 ◽  
pp. 27-35
Author(s):  
Alfonds Andrew Maramis ◽  
Mohamad Amin ◽  
Sumarno ◽  
Aloysius Duran Corebima
Keyword(s):  

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
M. Gokila Vani ◽  
K. J. Senthil Kumar ◽  
Jiunn-Wang Liao ◽  
Shih-Chang Chien ◽  
Jeng-Leun Mau ◽  
...  

In this study, we investigated the cytoprotective effects of antcin C, a steroid-like compound isolated from Antrodia cinnamaomea against AAPH-induced oxidative stress and apoptosis in human hepatic HepG2 cells. Pretreatment with antcin C significantly protects hepatic cells from AAPH-induced cell death through the inhibition of ROS generation. Furthermore, AAPH-induced lipid peroxidation, ALT/AST secretion and GSH depletion was significantly inhibited by antcin C. The antioxidant potential of antcin C was correlated with induction of antioxidant genes including, HO-1, NQO-1,γ-GCLC, and SODviatranscriptional activation of Nrf2. The Nrf2 activation by antcin C is mediated by JNK1/2 and PI3K activation, whereas pharmacologic inhibition of JNK1/2 and PI3K abolished antcin C-induced Nrf2 activity. In addition, AAPH-induced apoptosis was significantly inhibited by antcin C through the down-regulation of pro-apoptotic factors including, Bax, cytochrome c, capase 9, -4, -12, -3, and PARP.In vivostudies also show that antcin C significantly protected mice liver from AAPH-induced hepatic injury as evidenced by reduction in hepatic enzymes in circulation. Further, immunocytochemistry analyses showed that antcin C significantly increased HO-1 and Nrf2 expression in mice liver tissues. These results strongly suggest that antcin C could protect liver cells from oxidative stress and cell deathviaNrf2/ARE activation.


Sign in / Sign up

Export Citation Format

Share Document