scholarly journals Protective Effect of Lemon Peel Extract on Oxidative Stress in H9c2 Rat Heart Cell Injury

2021 ◽  
Vol Volume 15 ◽  
pp. 2047-2058
Author(s):  
Jun Wang ◽  
Yulin Zhai ◽  
Mingguang Ou ◽  
Yunfeng Bian ◽  
Chenglong Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Rat Heart ◽  
Cell Injury ◽  
Heart Cell ◽  
Lemon Peel ◽  
Peel Extract

scholarly journals In Vitro and In Vivo Inhibitory Effect of Citrus Junos Tanaka Peel Extract against Oxidative Stress-Induced Apoptotic Death of Lung Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1231
Author(s):  
Jin Woo Kim ◽  
Eun Hee Jo ◽  
Ji Eun Moon ◽  
Hanvit Cha ◽  
Moon Han Chang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Inhibitory Effect ◽  
Lung Cells ◽  
In Vivo Models ◽  
Citrus Junos ◽  
Induced Apoptosis ◽  
Peel Extract

Various stresses derived from both internal and external oxidative environments lead to the excessive production of reactive oxygen species (ROS) causing progressive intracellular oxidative damage and ultimately cell death. The objective of this study was to evaluate the protective effects of Citrus junos Tanaka peel extract (CE) against oxidative-stress induced the apoptosis of lung cells and the associated mechanisms of action using in vitro and in vivo models. The protective effect of CE was evaluated in vitro in NCI-H460 human lung cells exposed to pro-oxidant H2O2. The preventive effect of CE (200 mg/kg/day, 10 days) against pulmonary injuries following acrolein inhalation (10 ppm for 12 h) was investigated using an in vivo mouse model. Herein, we demonstrated the inhibitory effect of CE against the oxidative stress-induced apoptosis of lung cells under a highly oxidative environment. The function of CE is linked with its ability to suppress ROS-dependent, p53-mediated apoptotic signaling. Furthermore, we evaluated the protective role of CE against apoptotic pulmonary injuries associated with the inhalation of acrolein, a ubiquitous and highly oxidizing environmental respiratory pollutant, through the attenuation of oxidative stress. The results indicated that CE exhibits a protective effect against the oxidative stress-induced apoptosis of lung cells in both in vitro and in vivo models.

scholarly journals Protective effect of pineapple (Ananas cosmosus) peel extract on alcohol–induced oxidative stress in brain tissues of male albino rats

2011 ◽  
Vol 1 (1) ◽  
pp. 5-9 ◽  
Author(s):  
Ochuko L Erukainure ◽  
John A Ajiboye ◽  
Rachael O Adejobi ◽  
Oluwatoyin Y Okafor ◽  
Sunday O Adenekan
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Albino Rats ◽  
Peel Extract ◽  
Brain Tissues

Characterization of the Protective Effect of Tetrahydrobiopterin Against S-Nitroso-N -Acetyl-D ,L-Penicillamine Induced Endothelial Cell Injury

Pteridines ◽  
1999 ◽  
Vol 10 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Kazutaka Momose ◽  
Yuji Kiuchi ◽  
Toshinori Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Oxygen Species ◽  
No Donor ◽  
Endothelial Cell Injury ◽  
Ros Scavenger ◽  
Intracellular Oxidative Stress

The purpose of this study was to characterize the protective effect of tetrahydrobiopterin (BH4), one of the cofactors of nitric oxide (NO) synthase, against NO-induced endothelial cell injury. The addition of S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, to endothelial cells induced the release of lactate dehydrogenase (LDH), a marker for cell injury. The SNAP-induced endothelial cell injury was markedly reduced by pretreatment with sepiapterin, a precursor of BH4 synthesis. On the other hand, exogenous BH4 had little effect on the SNAP-induced endothelial cell injury. We recently found that NO-induced endothelial cell injury involves a part of H202 production, since the injury was blocked by the treatment with catalase. Although BH4 released reactive oxygen species (ROS) in cell-free conditions, the increase in intracellular BH4 by pretreatment with sepiapterin strongly reduced H202-induced intracellular oxidative stress. These findings suggest that the increase in intracellular BH4 content but not extracellular BH4, strongly attenuates NO-induced endothelial cell injury by at least one of the mechanisms by which BH4 reduces H202-induced oxidative stress. Intracellular BH4 seems mainly to play a role as an antioxidant or as a ROS-scavenger.

Protective effect of aqueous Curry leaf (Murraya koenigii) extract against cadmium-induced oxidative stress in rat heart

2012 ◽  
Vol 50 (5) ◽  
pp. 1340-1353 ◽  
Author(s):  
Elina Mitra ◽  
Arnab K. Ghosh ◽  
Debosree Ghosh ◽  
Debasri Mukherjee ◽  
Aindrila Chattopadhyay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Rat Heart ◽  
Murraya Koenigii

scholarly journals Protective Effect of Patchouli Alcohol Against SH-SY5Y Cell Injury Induced by Aβ25-35 via the Reduction of Oxidative Stress and Apoptosis

2021 ◽  
Vol 16 (7) ◽  
pp. 1934578X2110317
Author(s):  
Xie Yun-Liang ◽  
Zhang Bo
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Cell Injury ◽  
Lactic Dehydrogenase ◽  
Underlying Mechanism ◽  
Mtor Pathway ◽  
Protein Levels ◽  
Patchouli Alcohol ◽  
Injury Group ◽  
Phosphorylated Akt

Patchouli alcohol (PA) has multiple pharmacological activities, but its protective effect against SH-SY5Y cell injury induced by Aβ25-35 has not been reported. It has been recorded that phosphatidylinositol 3-hydroxykinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway plays an important role in neuroprotection. The purpose of this study was to investigate the protective effect of PA against SH-SY5Y cell injury induced by Aβ25-35 and its underlying mechanism. The results showed that compared with that in the Aβ25-35-induced injury group, the survival rate of SH-SY5Y cells increased ( P < .01) in the different PA-treated groups and the lactic dehydrogenase activity decreased significantly ( P < .01) in the 10, 20, and 40 μg/mL PA groups; compared with those in the Aβ25-35-induced injury group, the malonyldialdehyde contents in SH-SY5Y cells decreased ( P < .05 or P < .01), while the superoxide dismutase, glutathione peroxidase, and catalase activities increased significantly ( P < .05 or P < .01) in the different PA-treated groups; compared with those in the Aβ25-35-induced injury group, the apoptosis rates, and the mRNA and protein levels of Caspase-3 and Bax in SH-SY5Y cells decreased ( P < .05 or P < .01), while the mRNA and protein levels of Bcl-2, and phosphorylated Akt (p-Akt) and phosphorylated mTOR protein levels increased significantly ( P < .05 or P < .01) in the different PA-treated groups. The above results indicate that PA can inhibit the oxidative stress and apoptosis of SH-SY5Y cells induced by Aβ25-35 by regulating the PI3K/Akt/mTOR pathway, to protect the SH-SY5Y cells from the injury induced by Aβ25-35.

scholarly journals Protective Effect of Lemon Peel Polyphenols on Oxidative Stress-Induced Damage to Human Keratinocyte HaCaT Cells Through Activation of the Nrf2/HO-1 Signaling Pathway

2021 ◽  
Vol 7 ◽  
Author(s):  
Xi Gao ◽  
Diru Xu ◽  
Xinyue Zhang ◽  
Hengguang Zhao
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Western Blot ◽  
Protective Effect ◽  
Cell Survival ◽  
Hacat Cells ◽  
Model Group ◽  
Lemon Peel ◽  
Human Keratinocyte

Lemon peel can be used as traditional Chinese medicine. Flavonoids are the most important components in lemon peel, which can be developed as natural medicine without side effects. This study investigated the protective effect of lemon peel polyphenols (LPP) on human keratinocyte HaCaT cells under oxidative stress. The active components of LPP were determined by high performance liquid chromatography. The abilities of LPP to scavenge DPPH and ABTS+ free radicals were studied for detection of antioxidation in vitro. Cell survival rates were determined by MTT assay. The antioxidant enzyme activity and antioxidant index of cells were determined using kit. The mRNA and protein expression of cells were determined by qPCR and western blot. The ability of LPP to scavenge DPPH and ABTS+ free radicals were stronger than those of vitamin C (Vc) at the same concentration. As expected, compared with the normal group of cells, the model group had decreased cell survival, increased lactate dehydrogenase (LDH), decreased levels of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH), and increased malondialdehyde (MDA) content. qPCR and western blot results indicated that the expression of Bcl-2-related X protein (Bax), caspases-3, erythroid-derived nuclear factor 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) were decreased and the expression of B-cell lymphoma-2 (Bcl-2) was increased in the model group, compared with the normal group. LPP treatment improved cell survival rate, reduced intracellular LDH and MDA levels, increased intracellular SOD, CAT, GSH levels, down-regulated Bax, caspases-3, Nrf2, HO-1 expression, and up-regulated Bcl-2 expression. Component analyses found that LPP contains gallic acid, neochlorogenic acid, (+)-catechin, caffeic acid, (−)-Catechin gallate, isochlorogenic acid A, rosmarinic acid, and protocatechuic acid. LPP was found to regulate the Nrf2/HO-1 signaling pathway through 8 active substances to protect HaCaT cells against oxidative stress in vitro.

scholarly journals Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Fan Deng ◽  
Shuang Wang ◽  
Shuyun Cai ◽  
Zhe Hu ◽  
Riping Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Endothelial Cell ◽  
Cell Surface ◽  
Protective Effect ◽  
Cell Injury ◽  
Cellular Damage ◽  
Structural Protein ◽  
Surface Plasma ◽  
Antioxidative Stress

Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ-CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ-CD. EMVs released from H/R-treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning-suppressed microvesicles release and cell injury by H/R.

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