2013
DOI: 10.1016/j.bbadis.2013.07.008
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Glutathione and antioxidant enzymes serve complementary roles in protecting activated hepatic stellate cells against hydrogen peroxide-induced cell death

Abstract: Activated HSCs have increased ROS-detoxifying capacity compared to quiescent HSCs. Glutathione levels increase during HSC activation and protect against ROS-induced necrosis, whereas hydrogen peroxide-detoxifying enzymes protect against apoptotic cell death.

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Cited by 103 publications
(73 citation statements)
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“…4B and D). A similar phenomenon has been observed in rat hepatic stellate cells activated by hydrogen peroxide (H 2 O 2 ), in which the cellular GSH content is increased to protect against ROS, and the CAT protein expression is decreased, suggesting CAT might play a complementary role in the response to oxidative stress [27]. As shown in our results, EPA induced the cellular GSH content (Supplemental Fig.…”
Section: Discussionsupporting
confidence: 79%
“…4B and D). A similar phenomenon has been observed in rat hepatic stellate cells activated by hydrogen peroxide (H 2 O 2 ), in which the cellular GSH content is increased to protect against ROS, and the CAT protein expression is decreased, suggesting CAT might play a complementary role in the response to oxidative stress [27]. As shown in our results, EPA induced the cellular GSH content (Supplemental Fig.…”
Section: Discussionsupporting
confidence: 79%
“…The lower GSH level was also observed in this group. Therefore, lipid peroxidation in APAP toxicity was due to accumulation of H 2 O 2 following hepatic GSH depletion which leads to reduce efficacy of glutathione peroxidase [22] . Moreover, the tissue SOD level was also low in the APAP group.…”
Section: Discussionmentioning
confidence: 99%
“…The innate antioxidants such as SOD and the GSH, play an important role to counter-check the oxidative stress. The SOD neutralises the superoxide anions whereas the GSH is responsible to remove H 2 O 2 via glutathione peroxidase [22]. The cell injury in APAP toxicity is owing to the excess amount of unconjugated NAPQI which binds to the cellular protein of membranebound cytoplasmic organelles such as mitochondria, endoplasmic reticulum and the nucleus, resulting in impaired cellular function and cell death [20] .…”
Section: Discussionmentioning
confidence: 99%
“…However, it is still to be determined whether antifibrotic effects are due to the direct inhibitory action on hepatic stellate cells activation or by anti-oxidant potentials possessed by the extracts (Nimse et al, 2015;Van acker et al, 1996); since oxidative stress play crucial role in hepatic injury and hepatic stellate cell proliferation. (Dunning et al, 2013) Another possible mechanism of action can be related to the presence of steroidal constituents present in P. karka. Sultan et al, has reported the presence of steroidal moieties in P. karka (Sultan et al, 2017), which suggests its diversified effects on prostaglandin synthesis pathway.…”
Section: Discussionmentioning
confidence: 99%