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#28961281   2017/09/29 Save this To Up

Chronic administration of mitochondrion-targeted peptide SS-31 prevents atherosclerotic development in ApoE knockout mice fed Western diet.

Oxidative stress and inflammatory factors are deeply involved in progression of atherosclerosis. Mitochondrion-targeted peptide SS-31, selectively targeting to mitochondrial inner membrane reacting with cardiolipin, has been reported to inhibit ROS generation and mitigate inflammation. The present study was designed to investigate whether SS-31 could suppress the development of atherosclerosis in vivo.

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#28934742   2017/09/21 Save this To Up

Elevated Apoptosis in the Liver of Dairy Cows with Ketosis.

Dairy cows with ketosis are characterized by oxidative stress and hepatic damage. The aim of this study was to investigate hepatic oxidative stress and the apoptotic status of ketotic cows, as well as the underlying apoptosis pathway.

1868 related Products with: Elevated Apoptosis in the Liver of Dairy Cows with Ketosis.

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#28736364   2017/07/24 Save this To Up

[Angiotensin-(1-7) protects cardiac myocytes against high glucose-induced injury by inhibiting ClC-3 chloride channels].

To explore whether angiotensin-(1-7) [Ang-(1-7)] protects cardiac myocytes against high glucose (HG)-induced injury by inhibiting ClC-3 chloride channels.

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#28678311   2017/07/05 Save this To Up

Regulation of miR-92a on vascular endothelial aging via mediating Nrf2-KEAP1-ARE signal pathway.

Various human aging-related diseases start with vascular aging, in which the aging of vascular endothelium is the first step to cause a structural and functional deficit of vascular endothelium, leading to vascular disorders. MicroRNA (miR) participates in various processes of body development and pathological processes via mediating cell proliferation, differentiation, and apoptosis. A previous study showed the correlation between cardiovascular disease and miR-92a, whose role and mechanism in vascular endothelial aging has not been reported.

2024 related Products with: Regulation of miR-92a on vascular endothelial aging via mediating Nrf2-KEAP1-ARE signal pathway.

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#28635220   2017/06/21 Save this To Up

[The bisphenol A-enhanced activity of thyroid carcinoma cell line B-CPAP is inhibited by Icarrin].

Objective: To investigate the effect of icariin (ICA) on the bisphenol A (BPA)-enhanced proliferation function of thyroid carcinoma cell B-CPAP and underlying mechanism. Methods: The proliferation of Gastric B-CPAP cell line was evaluated by cell counting kit-8 (CCK-8). Apoptosis and ROS expression in B-CPAP cells were detected by flow cytometry. The expression of superoxide dismutase (SOD) and malondialdehyde (MDA) in B-CPAP cells were measured by individual assay kits. The expressions of Bcl-2 and γ-HA2X were detected by Western blot. SPSS 18.0 software was used to analyze the data. Results: B-CPAP cell activity was promoted by treatment with 3×10(-7)mol/L BPA for 48 h, with significant difference in absorbance between BPA and control groups (1.089±0.053 vs 0.935±0.010, P<0.05). The cell activities of BPA+ ICA(25), BPA+ ICA(50), BPA+ ICA(100) and BPA+ ICA(200) groups was 0.780±0.036, 1.007±0.050, 0.958±0.033 and 0.625±0.064, respectively (all P<0.01). The proliferation of B-CPAP cells treated with BPA for 72 hours showed a similar trend to 48 hours. There was no significant difference between all treatment groups in 24 hours. The apoptosis rate was (19.272±0.186)% in BPA-treated cells, and was (22.412±0.238)% in control cells (P<0.05). The apoptosis rates of BPA+ ICA(50) and BPA+ ICA(200) groups were (23.688±0.412)% and (30.270±0.696)%, respectively (P<0.01). The intracellular accumulation of ROS in BPA, BPA+ ICA(50), and BPA+ ICA(200) groups were 806±21, 1 772±37, 2 041±16, respectively (P<0.01). The expressions of anti-apoptotic protein Bcl-2 in control, BPA, BPA+ ICA(50), BPA+ ICA(200) groups were 7 120±151, 9 801±286, 5 902±171 and 4 203±216, respectively (P<0.01). Conclusion: BPA can promote the proliferation of thyroid carcinoma B-CPAP cells and decrease the apoptosis of cells, and this effect can be inhibited by ICA. The possible mechanism is to induce high expression of intracellular ROS and inhibit the expression of antioxidase system, leading to cell oxidative damage, thereby inducing apoptosis.

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#28502304   2017/05/15 Save this To Up

[Inula Britannica flower total flavonoids reduces the apoptosis of aging bone marrow mesenchymal stem cells by anti-oxidation].

Objective To investigate the beneficial effect of Inula Britannica flower total flavonoids (IBFTF) on aging bone mesenchymal stem cell (BMSC) and its potential mechanism. Methods The aging BMSCs were induced by D-galactose, and then treated with 12.5, 25, 50 μg/mL IBFTF. The cell viability was detected by CCK-8 assay. The activity of catalase (CAT) and superoxide dismutase (SOD), the content of malondialdehyde (MDA) and reactive oxygen species (ROS) were measured by a commercial kit. The apoptosis was assessed by flow cytometry. The protein expressions of BAX, Bcl-2 and cleaved-caspase-3 (c-caspase-3) were determined by Western blotting. Results The cell viability and the activity of SOD and CAT in the aging group decreased significantly compared with the normal group, whereas different concentrations of IBFTF promoted the cell viability, and simultaneously increased the activity of SOD and CAT. The apoptosis, the ROS production, the content of MDA, BAX/Bcl-2 ratio and the protein expression of c-caspase-3 in the aging group increased obviously compared with the normal group. However, the treatment of different concentrations of IBFTF reduced the apoptosis, the ROS production, the content of MDA, BAX/Bcl-2 ratio and the protein expression of c-caspase-3. Conclusion IBFTF can attenuate the apoptosis of aging BMSCs by anti-oxidation.

1842 related Products with: [Inula Britannica flower total flavonoids reduces the apoptosis of aging bone marrow mesenchymal stem cells by anti-oxidation].

FDA Standard Frozen Tissu FDA Standard Frozen Tissu Rat Mesenchymal Stem Cell Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Macrophage Colony Stimula Macrophage Colony Stimula Anti 3 DG imidazolone Mon Anti AGE 3 Monoclonal Ant Rat Mesenchymal Cells

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#28443516   2017/04/26 Save this To Up

Synergistic effect of graphene oxide coated nanotised apigenin with paclitaxel (GO-NA/PTX): A ROS dependent mitochondrial mediated apoptosis in ovarian cancer.

Ovarian cancer is most lethal among all gynecologic malignancies. Paclitaxel (PTX) is well used chemotherapeutic regimen for cancer control; however its undesired toxicity has been always a matter of concern for clinicians. Here we used the graphene oxide coated nanotised apigenin (GO-NA) as chemo sensitizing agent to enhance the efficacy of paclitaxel to overcome the limitations of chemotherapy. GO and GO-Apigenin was prepared by modified Hummers method and the nanoparticles were characterized by dynamic light scattering and transmission electron microscopy Human ovarian adenocarcinomas (SKOV-3) cells was treated by DMSO, Group I (Control)-McCoy's 5A Medium, Group II-Paclitaxel (5nM) alone, Group III- Nanotised Apigenin (GO-NA-10μM) Group IV- Paclitaxel (5nM) + GO-NA (10μM). Cell viability and IC-50 value were determined by MTT assay, synergism by Compusyn software, ROS by DCFH-DA assay, SOD activity by commercially available kit and MMP were examined by JC-1 and mitotracker/DAPI staining, cell cycle by flow cytometry, mRNA and protein level of apoptotic molecules caspase-3, Bax, and Bcl-2 were detected by Real Time-PCR and Western blot respectively. Results showed that GO-NA-PTX dramatically enhanced the anti-proliferative effect in synergistic manner as compare to GO-NA and PTX alone. GO-NA-PTX significantly suppressed the SOD activity, promotes the ROS accumulation, mitochondrial depolarization, DNA integrity and cell cycle arrest collectively accord the apoptotic cell death. In addition, results of immunocytochemistry, RT-PCR and western blot also supported the apoptosis by up-regulating the bax, caspase3 and down-regulation of Bcl2. Conclusively, our data showed the GO-NA-PTX may be a promising method for ovarian cancer chemotherapy.

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#28431381   2017/04/21 Save this To Up

Zeaxanthin ameliorates high glucose-induced mesangial cell apoptosis through inhibiting oxidative stress via activating AKT signalling-pathway.

Oxidative stress is a critical factor in the pathophysiology of diabetic kidney disease. Previous study shows that hyperglycaemia aggravates renal injury through oxidative stress in diabetic model, and antioxidants have beneficial effect on diabetic kidney disease. However, the role of antioxidants in the progression of diabetic kidney disease is poorly understood. The aim of this study was to clarify whether zeaxanthin, an antioxidant, could ameliorate mesangial cell injury and if so, identify the related mechanism underlying this protective effect. To that end, superoxide dismutase (SOD) activity and methane dicarboxylic aldehyde (MDA) levels were measured by an assay kit, and mesangial cell apoptosis and ROS levels were assessed using flow cytometry analysis. Furthermore, The levels of a phosphorylated ser/thr protein kinase (p-AKT), phosphorylated glycogen synthase kinase-3 beta (p-GSK-3β), Bcl-2 associated X protein (Bax) and cleaved cysteinyl aspartate-specific proteinase-3 (caspase-3) were detected by western blot. We found that zeaxanthin decreases MDA levels and increased SOD activity, as well as inhibits apoptosis and decreases ROS levels in mesangial cells in a high sugar environment. Furthermore, zeaxanthin increased p-AKT levels while decreased the levels of p-GSK-3β, Bax and cleaved-caspase-3. In addition, LY294002 reversed the protective effect of zeaxanthin on mesangial cells. In conclusion, zeaxanthin ameliorated mesangial cell apoptosis may be involved in inhibiting oxidative stress through activating of the AKT signalling pathway.

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#28386344   2017/04/07 Save this To Up

GYY4137 stimulates osteoblastic cell proliferation and differentiation via an ERK1/2-dependent anti-oxidant mechanism.

Oxidative stress plays a critical role in the development of osteoporosis. Hydrogen sulfide (H2S), produces anti-oxidant effect in various biological systems. The present study found that GYY4137, a slow H2S releasing compound, stimulated both mRNA level and activity of alkaline phosphatase, the marker of osteoblast differentiation. This research aims to explore the mechanism on how GYY4137 stimulates osteoblastic cell proliferation and differentiation via an ERK1/2-dependent anti-oxidant approach.

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#28359892   2017/03/31 Save this To Up

Bamboo leaf extract ameliorates diabetic nephropathy through activating the AKT signaling pathway in rats.

Diabetic nephropathy (DN) is one of the most severe diabetic complication and it is becoming become a worldwide epidemic, accounting for approximately one-third of all case of end-stage renal disease. However, the underlying mechanism and strategy to alleviate renal injury remain unclear. In the present study, we assessed the protective effect of bamboo leaf extract on the DN, and investigated the underlying mechanism by which bamboo leaf extract ameliorating DN. Diabetic rats were induced by 4 weeks high sugar and high fat diet, and then injected a single dose of STZ (35mg/kg) into abdominal cavity. Different dose of bamboo extract (50mg/kg, 100mg/kg and 200mg/kg) were orally administered every day for a period of 12 weeks. Body weight, blood glucose, glycosylated hemoglobin A1c (HbAlc), blood urea nitrogen (BUN), serum creatinine (Scr), and 24-hour urinary protein (24 h-UP) were assessed. Total superoxide dismutase (T-SOD) activity and MDA (methane dicarboxylic aldehyde, MDA) level were tested by assay kit. Microstructural changes were observed by hematoxylin-eosin (HE) staining and electron microscopy. Expression of phosphorylated ser/thr protein kinase (P-AKT), phosphorylated glycogen synthase kinase-3 beta (P-GSK-3β), B cell lymphoma/leukemia 2-associated X protein (BAX) and cleaved-cysteinyl aspartate-specific proteinase-3 (Cleaved Caspase-3) were measured by Western-Blotting (WB). Results showed that diabetic rats had weight loss, high blood glucose, HbAlc, BUN, Scr and 24-UP and T-SOD activity were increased and MDA level was decreased in diabetic rats. Moreover, hyperglycemia could injury renal tissue ultrastructure, inhibit P-AKT level and increase P-GSK-3β, BAX and Cleaved Caspase-3 levels in rats. However, bamboo leaf extract treatment could reduce body weight loss, BUN, Scr, 24 h-UP and MDA level, improve T-SOD activity and alleviate renal injury in diabetic rats. Furthermore, bamboo leaf extract increased P-AKT level, decreased P-GSK-3β, BAX and Cleaved Caspase-3 levels in STZ-diabetic rats. In conclusion, our study suggested that bamboo leaf extract ameliorated DN in diabetic rats, and this protective effect is possibly related to suppressing oxidative stress through activating AKT signaling pathway. Bamboo leaf extract treatment may be a potential promising therapy for DN.

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