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[Experimental observation of hyperbaric oxygen combined with radioactive seed implantation in the treatment of nude mice bearing esophageal squamous cell carcinoma].

Objective: To investigate the effect and mechanism of hyperbaric oxygen combined with radioactive seed implantation in the treatment of esophageal squamous cell carcinoma. Methods: Subcutaneous tumor model of esophageal squamous cell carcinoma using TE-8 cells was established. Tumor bearing Balb/c(nu/nu) mice (60 mice) were divided into four groups, Cont group that treated with normal oxygen level, HBO group that treated with hyperbaric oxygen, RSI group that treated with radioactive seed implantation, and HBO+ RSI group that treated with hyperbaric oxygen combined with radioactive seed implantation. Tumor volume ratio and mean survival time of tumor bearing mice were observed. Pathological changes of tumor tissue after treatment were observed by hematoxylin eosin (HE) staining. Enzyme linked immunosorbent assay kit was used to detect oxidative stress. Apoptosis related proteins were detected by Western blot. Results: After treatment, the tumor volume ratio of HBO+ RSI group was 3.51±0.80 and was significantly lower than that of Cont group, HBO group, and RSI group (P<0.05). The mean survival time of HBO+ RSI group tumor bearing mice was 62 d and was significantly longer than that in Cont group, HBO group, and RSI group (P<0.05). HE staining showed that the pathological changes of tumor tissues were most obvious in HBO+ RSI group. After treatment, the MDA and Bax levels in nude mice of HBO+ RSI group were significantly higher than those in Cont group, HBO group and RSI group, but the levels of GSH, SOD and Bcl-2 were significantly lower than those of Cont group, HBO group and RSI group (P<0.05). Conclusion: Hyperbaric oxygen combined with radioactive seed implantation could slow tumor growth and increase survival time of tumor bearing mice. The possible mechanism is that hyperbaric oxygen combined with radioactive seed implantation can improve the oxidative stress response and the expression of apoptosis protein in tumor bearing nude mice.

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Esophageal squamous cell Esophageal squamous cell Lung squamous cell carcin Cervix squamous cell carc Esophagus squamous cell c Esophagus squamous cell c Esophageal squamous cell Esophageal squamous cell Esophagus squamous cell c Oral cavity squamous cell Skin squamous cell carcin Multiple organ squamous c

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Overexpression of miR-22 attenuates oxidative stress injury in diabetic cardiomyopathy via Sirt 1.

Oxidative stress injury is believed to be important in diabetic cardiomyopathy. Recent evidence indicates that miR-22 plays an important role in various cardiovascular diseases, but the protective role of miR-22 in diabetic cardiomyopathy remains undetermined.

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Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis.

Alzheimer's disease (AD) is an age-related neurodegenerative disease linked with increased production and/or deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective effect of troxerutin on an animal model of Alzheimer's disease. Alzheimer model was induced by a single dose intracerebroventricular (ICV) injection of Aβ 1-42 (5 nmol/5 µl). Thereafter, troxerutin (300 mg/kg) was gavaged for 14 days. The hippocampal malondialdehyde (MDA) levels and enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) were measured using enzyme-linked immunosorbent assay (ELISA) method. In addition, the number of apoptotic cells in the dentate gyrus (DG) was assessed by TUNEL kit. The results showed that ICV microinjection of Aβ 1-42 increased MDA levels, reduced SOD and GPx, and increased AChE activities in the hippocampus. Chronic administration of troxerutin significantly attenuated MDA levels and AChE activity and increased SOD and GPx activities in the hippocampus. Moreover, the number of apoptotic cells was decreased by troxerutin treatment. Taken together, our study demonstrated that troxerutin could increase the resistance of hippocampal neurons against apoptosis, at least in part, by diminishing the activity of AChE and oxidative stress. Therefore, troxerutin may have beneficial effects in the management of Alzheimer's disease.

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Potential role of S100A8 in skin rejuvenation with the 1064-nm Q-switched Nd:YAG laser.

The 1064-nm Q-switched Nd:YAG laser is demonstrated to be effective for non-ablative skin rejuvenation, but the molecular mechanism by which dermis responses to laser-induced damage and initiates skin remodeling is still unclear. HaCaT cells and 3T3 skin fibroblasts were irradiated with the 1064-nm Q-switched Nd:YAG laser at the different doses. Then, cells were collected and lysed for PCR and Western blot analysis. Cell viability was detected by Cell Counting Kit-8 (CCK-8) before and after laser irradiation. The expressions of S100A8, advanced glycosylation end product-specific receptor (RAGE) and inflammatory cytokines in two cell lines were markedly upregulated after laser treatments. The PCR, Western blot, and ELISA analysis showed the significant increase of type I and III procollagen in the 3T3 cells treated with the 1064-nm laser. Interestingly, si S100A8 effectively inhibited the expression of cytokines and collagen, while S100A8 treatments significantly increased them. P-p38 and p-p65 levels were also elevated after the 1064-nm laser irradiation, which is positively related with S100A8. Cell viability and reactive oxygen species (ROS) levels were not changed, while the content of superoxidase dismutase (SOD) in two cells was increased after laser irradiation. Our results demonstrated that the overexpression of S100A8 induced by the 1064-nm laser irradiation triggered inflammatory reactions in skin cells. The inflammatory microenvironment and improvement of skin antioxidant capacity contribute to new collagen synthesis in the skin cells. Thus, S100A8 was required for laser-induced new collagen synthesis in skin cells. p38/MAPK and NF-κB signal pathways were involved in S100A8-mediated inflammatory reactions in response to laser irradiation.

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Protective effect of GDNF-engineered amniotic fluid-derived stem cells on the renal ischaemia reperfusion injury in vitro.

Amniotic fluid-derived stem cells (AFSCs) possessing multilineage differentiation potential are proposed as a novel and accessible source for cell-based therapy and tissue regeneration. Glial-derived neurotrophic factor (GDNF) has been hypothesized to promote the therapeutic effect of AFSCs on markedly ameliorating renal dysfunction. The aim of this study was to investigate whether AFSCs equipped with GDNF (GDNF-AFSCs) had capabilities of attenuating mouse renal tubular epithelial cells (mRTECs) apoptosis and evaluate its potential mechanisms.

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Macrophage Colony Stimula Macrophage Colony Stimula anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Human Glial Derived Neuro GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog C Peptide ELISA Kit, Rat Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep Cultrex In Vitro Angiogen

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Resveratrol Attenuates the Cytotoxicity Induced by Amyloid-β1-42 in PC12 Cells by Upregulating Heme Oxygenase-1 via the PI3K/Akt/Nrf2 Pathway.

Oxidative stress and cytotoxic damage induced by amyloid beta (Aβ) have been considered pivotal in the pathogenesis of Alzheimer's disease (AD) and may represent a target for treatment. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway elicits a survival signal to protect against multiple injuries, and the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a downstream target of the PI3K/Akt pathway, can bind to HO-1. Resveratrol, a natural polyphenol derived from grapes, has been widely reported to have diverse antioxidative effects against AD, but the mechanisms have not been fully elucidated. The present study aims to investigate the effects of resveratrol on Aβ1-42-induced cytotoxicity in PC12 cells and to explore the potential mechanisms of these effects. PC12 cells were cultured and treated with Aβ1-42. Oxidative stress was assessed by measuring malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) levels. After treating with resveratrol at different concentrations (0, 10, 20, 40 μM) and for different durations (24, 48, 72 h), the generation of MDA, GSH, and SOD were detected; cell viability was assessed by MTT assay. The production of reactive oxygen species (ROS) was determined using an ROS Assay Kit. Western blotting was used to detect the protein expression. Our studies showed that pretreatment with resveratrol could reduce Aβ1-42-induced oxidative stress in PC12 cells by inhibiting the generation of MDA and ROS and increasing the production of SOD and GSH. Resveratrol markedly attenuated the Aβ1-42-induced loss in cell viability in PC12 cells in both a dose- and time-dependent manner. More importantly, resveratrol stimulated the activation of HO-1, Nrf2, PI3K, and phosphorylated Akt. Notably, the neuroprotective effects of resveratrol were eliminated by the HO-1 inhibitor zinc protoporphyrin IX (ZnPP), Nrf2 small interfering RNA (siRNA), and the PI3K/Akt inhibitor LY294002. Taken together, the findings suggest that the cytoprotection of resveratrol against the cytotoxicity induced by Aβ1-42 in PC12 cells is through the upregulation of HO-1 expression via the activation of the PI3K/AKT/Nrf2 intracellular signaling pathway, which might provide novel insights for understanding the mechanism of the neuroprotective effect of resveratrol as an anti-AD drug.

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BYL-719 Mechanisms: PI3K- AKT Phospho-Specific Arra Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Macrophage Colony Stimula anti H inh human blood an TCP-1 theta antibody Sour TGF beta induced factor 2 Recombinant Thermostable Recombinant Human PKC the

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[Grain-Moxibustion may Protect Myocardium by Reducing Oxidative Stress in Doxorubicin-induced Cardiomyopathy Rats].

To observe the effectiveness of grain-moxibustion in resisting oxidative stress in doxorubicin (DOX)-induced cardiomyopathy rats.

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The protective effects of ischemic preconditioning on rats with renal ischemia-reperfusion injury and the effects on the expression of Bcl-2 and Bax.

The aim of the present study was to investigate the protective effects of ischemic preconditioning on rats with renal ischemia-reperfusion injury and the effects on the expression of Bcl-2 and Bax. Thirty-six SD rats were randomly divided into three groups (n=12) including sham operation (S) group, ischemia-reperfusion group (I/R) group and ischemic preconditioning (IP) group. After anesthesia with intraperitoneal injection of chloral hydrate, bilateral renal pedicles were clipped for 45 min, followed by perfusion for 6 h to establish the I/R model. Both kidneys in rats of S group were separated and exposed for 45 min, but renal pedicles were not clipped. In IP group, bilateral renal pedicles were clipped for 5 min, followed by perfusion for 5 min, this procedure was repeated 3 times. Then bilateral renal pedicles were clipped for 45 min, followed by perfusion for 6 h. Blood samples were collected and rats were sacrificed to collect renal tissue. Levels of serum creatinine (Cr) and blood urea nitrogen (BUN) were measured. Activity of superoxide dismutase (SOD) was measured by xanthine oxidase assay. Degree of renal injury was evaluated by H&E staining. TUNEL kit was used to detect the number of apoptotic cells in renal tissue. Expression levels of Bcl-2 and Bax were detected by semi-quantitative PCR and western blot analysis at mRNA and protein levels, respectively. Results showed that levels of Cr and BUN in I/R and IP groups were significantly higher than those in S group, and levels of Cr and BUN in I/R group were significantly higher than that in IP group (P<0.05). Activity of SOD in I/R group and IP group were significantly lower than those in S group, and activity of SOD in I/R group were significantly lower than those in IP group (P<0.05). H&E staining showed that, compared with S group, renal injury in the I/R and IP groups was more serious than that in the S group, and I/R group was more serious than the IP group (P<0.05). TUNEL apoptosis assay showed that number of apoptotic cells in IP and I/R groups were significantly higher than that in the S group (P<0.01). Semi-quantitative PCR and western blot analysis showed that, compared with the S group, expression levels of Bcl-2 mRNA and protein were significantly decreased, expression levels of Bax mRNA and protein were significantly increased, and the ratio of Bcl-2/Bax was significantly decreased in the IP and I/R groups (P<0.01). Compared with the I/R group, expression level of Bcl-2 was significantly increased, the level of Bax was significantly deceased, and the ratio of Bcl-2/Bax was significantly increased in the IP group (P<0.01). As a result, ischemic preconditioning can protect rats with renal ischemia-reperfusion injury possibly by increasing the expression level of Bcl-2 and decreasing the expression level of Bax.

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Edaravone Attenuates the Proinflammatory Response in Amyloid-β-Treated Microglia by Inhibiting NLRP3 Inflammasome-Mediated IL-1β Secretion.

Microglial activation is an important pathological feature in the brains of patients with Alzheimer's disease (AD), and amyloid-β (Aβ) peptides play a crucial role in microglial activation. In addition, edaravone (EDA) was recently shown to suppress oxidative stress and proinflammatory cytokine production in APPswePS1dE9 (APP/PS1) mice. However, the mechanism by which EDA inhibits the Aβ-induced proinflammatory response in microglia is poorly understood.

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CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7 Human Interleukin-2 IL-2 Human Interleukin-16 IL-1 Human Interleukin-33 IL-3 Human Interleukin-17E (IL Human Interleukin-32 alph Human Interleukin-17F IL- Human Interleukin-17AF He Human Epstein-Barr Virus

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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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