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#29270590   // Save this To Up

[Antioxidant effects of celastrol against hydrogen peroxide-induced oxidative stress in the cell model of amyotrophic lateral sclerosis].

To investigate the anti-oxidative effect of celastrol on H2O2-induced oxidative stress in the cell model of amyotrophic lateral sclerosis (ALS) and its molecular mechanism, NSC34 motor neuron-like cells were transfected with EGFP-G93A-SOD1 plasmid and used as in vitro ALS cell model. SOD1G93A transfected NSC34 cells were treated with different doses of H2O2 and celastrol. The survival rate of the cells was detected by CCK-8 assay, and malondialdehyde (MDA) content was detected by corresponding kit. The mRNA expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione S-transferases (GST) were detected by real-time PCR. The activation of intracellular MEK/ERK and PI3K/Akt signal pathways was detected by Western blot. The results showed that pre-incubation of celastrol (50 nmol/L) for 4 h prior to H2O2 (10 μmol/L) co-treatment for another 24 h significantly attenuated H2O2-induced cell death and MDA level in SOD1G93A transfected NSC34 cells. Real-time PCR showed that the mRNA expressions of GCLC and GST were enhanced with pre-incubation of celastrol. Celastrol quickly induced phosphorylation of ERK1/2 and Akt within 30 min and 1 h respectively in SOD1G93A transfected NSC34 cells. Pharmacological inhibitors of MEK (PD98059, 10 μmol/L) or Akt (MK2206, 10 μmol/L) could reverse the phosphorylation of ERK1/2 and Akt, and abolish up-regulation of GCLC and GST induced by celastrol at mRNA levels. Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1G93ANSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation.

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Increased MMAB level in mitochondria as a novel biomarker of hepatotoxicity induced by Efavirenz.

Efavirenz (EFV), a non-nucleoside reverse transcriptase inhibitor (NNRTI), has been widely used in the therapy of human immunodeficiency virus (HIV) infection. Some of its toxic effects on hepatic cells have been reported to display features of mitochondrial dysfunction through bioenergetic stress and autophagy, etc. However, alteration of protein levels, especially mitochondrial protein levels, in hepatic cells during treatment of EFV has not been fully investigated.

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[Effect and related mechanism of miRNA-21 on hydrogen peroxide-induced C-kit(+) cardiac stem cells apoptosis].

Objective: To explored the effect and related mechanism of miRNA-21 on hydrogen peroxide-induced C-kit(+) cardiac stem cells apoptosis. Methods: C-kit(+) cardiac stem cells were isolated from SD rats by the methods of enzyme digestion and magnetic bead. Cells were divided into the following experimental groups: (1) negative control mimics (NCM)group: cells were transfected with negative control miRNA-21 mimics for 48 hours; (2)mimics group: cells were transfected with miRNA-21 mimics for 48 hours; (3) NCM+ H(2)O(2) group: negative control miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H(2)O(2) for 2 hours; (4)mimics+ H(2)O(2) group: miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H(2)O(2) for 2 hours. mRNA of miRNA-21 was detected by RT-PCR. The apoptosis rate of C-kit(+) cardiac stem cells was determined using the annexin V-FITC/PI staining assay. Western blot was employed to measure the expression of apoptosis related proteins(Caspase-3, Bax, and Bcl-2). Results: (1) Compared with the NCM group, the mRNA expression level of miRNA-21 was significantly up-regulated in mimics group, while obviously down-regulated in NCM+ H(2)O(2) group(all P<0.05). Compared with the mimics group, the mRNA expression levels of miRNA-21 in mimics+ H(2)O(2) group was significantly downregulated (P<0.05), but remarkably upregulated compared with the NCM+ H(2)O(2) group(P<0.05). (2) Flow cytometry results indicated that the early apoptosis rates were similar between the NCM group and mimics group ((4.57±3.45)% vs. (5.13±3.21)%, P>0.05). Compared with the NCM group, the early apoptosis rates were remarkably increased ((79.07±5.75)% vs.(4.57±3.45)%, P<0.05) in NCM+ H(2)O(2) group. Compared with the mimics group, the early apoptosis was significantly up-regulated in the mimics+ H(2)O(2) group ((30.27±1.36)% vs.(5.13±3.21)%, P<0.05), which were further down-regulated in mimics+ H(2)O(2) group compared with the NCM+ H(2)O(2) group ((30.27±1.36)% vs.(79.07±5.75)%, P<0.05). (3) Western blot results showed similar protein expression of Caspase-3, Bax and Bcl-2 between NCM group and mimics group(all P>0.05). Compared with the NCM group, the Caspase-3 and Bax protein expression was significantly increased in NCM+ H(2)O(2) group (all P<0.05), but the protein expression level of Bcl-2 was similar between the 2 groups(P>0.05). The Caspase-3 and Bax protein expression was markedly decreased, while Bcl-2 apparently increased in the mimics+ H(2)O(2) group compared with the NCM+ H(2)O(2) group(all P<0.05). Conclusion: Overexpression of miRNA-21 protects the C-kit(+) cardiac stem cells from apoptosis caused by oxidative stress through downregulating proapoptotic and upregulating the antiapoptotic proteins.

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Diazoxide prevents H2O2-induced chondrocyte apoptosis and cartilage degeneration in a rat model of osteoarthritis by reducing endoplasmic reticulum stress.

Osteoarthritis (OA) is a common disease affecting elderly individuals. Its incidence rises sharply with age, and chondrocyte apoptosis plays a vital role in its pathogenesis. Diazoxide opens mitochondrial ATP-sensitive potassium (mitoKATP) channels and exerts multiple pharmacological effects, including reductions in blood pressure and blood sugar levels. It also exerts anti-apoptotic activities, but the cellular and molecular mechanisms by which diazoxide inhibits chondrocyte apoptosis are unknown, as is whether apoptosis is related to endoplasmic reticulum stress (ERS). In the present study, we explored the mechanism underlying the chondroprotective effect of diazoxide on hydrogen peroxide (H2O2)-stimulated chondrocyte apoptosis in rats with surgically induced OA. A cell counting kit-8 (CCK-8) assay showed that the viability of H2O2-stimulated chondrocytes was enhanced in a dose-dependent manner. However, at a concentration ≥400μM, diazoxide had other, negative effects. The protective effect of diazoxide in vitro included inhibition of the ERS response and of mitochondrial dysfunction induced by H2O2 stimulation. These responses were related to activation of the PERK1/2 and ERK1/2 signaling pathways; the prevention of chondrocyte apoptosis; the down-regulation of caspase-3, Bax, ATF-6 and C/EBP-homologous protein (CHOP) expression; and the up-regulation of Bcl-2 and Col II. In vivo, histological and immunohistochemical analyses of caspase-3 and CHOP expression revealed that diazoxide ameliorated cartilage degeneration in a rat model of OA, as revealed by histological and immunohistochemical analyses of caspase-3 and CHOP expression. Diazoxide suppressed H2O2-triggered chondrocyte apoptosis, and ameliorated cartilage degeneration, by inhibiting the development of ERS.

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Protective Effect of Combined Caffeic Acid Phenethyl Ester and Bevacizumab Against Hydrogen Peroxide-Induced Oxidative Stress in Human RPE Cells.

This study aimed to evaluate the protective effects of caffeic acid phenethyl ester (CAPE) and combined CAPE-bevacizumab against oxidative stress induced by hydrogen peroxide (H2O2) in human retinal pigment epithelium.

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Isoflurane Preconditioning Alleviated Murine Liver Ischemia and Reperfusion Injury by Restoring AMPK/mTOR-Mediated Autophagy.

Isoflurane has a pharmacological preconditioning effect against ischemia injury in the heart, kidney, and brain, but whether and how isoflurane preconditioning protects livers against ischemia and reperfusion (IR) injury is unclear.

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Salvianolic acid B protects hepatocytes from H2O2 injury by stabilizing the lysosomal membrane.

To investigate the capability of salvianolic acid B (Sal B) to protect hepatocytes from hydrogen peroxide (H2O2)/carbon tetrachloride (CCl4)-induced lysosomal membrane permeabilization.

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Chitosan oligosaccharides protect nucleus pulposus cells from hydrogen peroxide-induced apoptosis in a rat experimental model.

Chitosan has been investigated for its protective effect on nucleus pulposus (NP) cells against intervertebral disc degeneration(IDD), but its high molecular weight prohibits its clinical application. The low molecular derivatives, chitosan oligosaccharides (COS) are easier to absorb; however, the protective effect of COS against IDD remains unclear. In this study, we investigated the effects of COS on NP degeneration. NP cells derived from rats were treated with H2O2 to induce an IDD-like transition. Then, COS was used to pre-treat cells before administering H2O2 and changes occurring in the cells were observed. As shown by the result of a cell counting kit-8(CCK-8) assay, COS protected the viability of the cells. The induced apoptosis rate fell when cells were pre-treated with COS, revealed by annexin-V FITC/PI double staining analysis and Hoechst 33342 staining. COS administration also protected ECM synthesis and prevented its degradation, as shown by western blotting(WB) and polymerase chain reaction(PCR). We analyzed the activity of the PI3K/Akt pathway in H2O2 treated NP cells by WB and the result showed that COS could enhance activity of the pathway. To investigate the relationship between the PI3K/Akt pathway and the protective effects of COS on NP cells, the PI3K/Akt pathway was inhibited by wortmannin, and we subsequently found that this abolished the protective effects. These results support the hypothesis that COS exerts its protective effect on NP cells against H2O2-induced apoptosis via the PI3K/Akt pathway.

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Development of a H2 O2 -sensitive quantum dots-based fluorescent sandwich ELISA for sensitive detection of bovine β-lactoglobulin by monoclonal antibody.

Bovine β-lactoglobulin (BLG) is the major allergen in cows' milk, and the specific epitope plays a key role in food allergy. Developing a method specifically bind to the IgE epitope is necessary for testing BLG and its allergenic residues.

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Protective effects of Oviductus Ranae-containing serum on oxidative stress-induced apoptosis in rat ovarian granulosa cells.

Oviductus Ranae (OR) is a traditional Chinese medicine derived from Rana temporaria chensinensis David, and is known to have a wide variety of pharmacological effects.

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