scholarly journals Neuroprotective Potency of Tofu Bio-Processed Using Actinomucor elegans against Hypoxic Injury Induced by Cobalt Chloride in PC12 Cells

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2983
Author(s):  
Liqing Yin ◽  
Yongzhu Zhang ◽  
Fidelis Azi ◽  
Mekonen Tekliye ◽  
Jianzhong Zhou ◽  
...  
Keyword(s):  
Protective Effect ◽  
Pc12 Cells ◽  
Cobalt Chloride ◽  
Lactic Dehydrogenase ◽  
Phase Cell ◽  
Caspase 9 ◽  
Hypoxic Injury ◽  
Cell Arrest ◽  
Significant Protective Effect

Fermented soybean products have attracted great attention due to their health benefits. In the present study, the hypoxia-injured PC12 cells induced by cobalt chloride (CoCl2) were used to evaluate the neuroprotective potency of tofu fermented by Actinomucor elegans (FT). Results indicated that FT exhibited higher phenolic content and antioxidant activity than tofu. Moreover, most soybean isoflavone glycosides were hydrolyzed into their corresponding aglycones during fermentation. FT demonstrated a significant protective effect on PC12 cells against hypoxic injury by maintaining cell viability, reducing lactic dehydrogenase leakage, and inhibiting oxidative stress. The cell apoptosis was significantly attenuated by the FT through down-regulation of caspase-3, caspases-8, caspase-9, and Bax, and up-regulation of Bcl-2 and Bcl-xL. S-phase cell arrest was significantly inhibited by the FT through increasing cyclin A and decreasing the p21 protein level. Furthermore, treatment with the FT activated autophagy, indicating that autophagy possibly acted as a survival mechanism against CoCl2-induced injury. Overall, FT offered a potential protective effect on nerve cells in vitro against hypoxic damage.

Identification of miRNAs Involved in the Protective Effect of Sevoflurane Preconditioning Against Hypoxic Injury in PC12 Cells

2015 ◽  
Vol 35 (8) ◽  
pp. 1117-1125 ◽  
Author(s):  
Yingying Sun ◽  
Yuanhai Li ◽  
Lei Liu ◽  
Yiqiao Wang ◽  
Yingjing Xia ◽  
...  
Keyword(s):  
Protective Effect ◽  
Pc12 Cells ◽  
Hypoxic Injury ◽  
Sevoflurane Preconditioning

Protective effect of dihydromyricetin on vascular smooth muscle cell apoptosis induced by hydrogen peroxide in rats

Perfusion ◽  
2022 ◽  
pp. 026765912110599
Author(s):  
Wenling Li ◽  
Hua Sang ◽  
Xin Xu ◽  
Yuanyuan Zhang ◽  
Xiangying Meng ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Protective Effect ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Ros Scavenging ◽  
Caspase 9

Objective Dihydromyricetin (DMY), also called Ampelopsin, which was extracted from Ampelopsis grossedentata, has been demonstrated to have a protective effect against cell oxidative injury and cell apoptosis in vitro. In the present study, we tried to study the role of DMY on apoptosis of vascular smooth muscle cells (VSMCs) induced by hydrogen peroxide (H2O2) and explore the underlying mechanisms. Methods Apoptotic cells were detected by Hematoxylin and Eosin (H.E.) staining, Hoechst 33342 staining, and Annexin V-fluorescein isothiocyanate binding assay. The intracellular reactive oxygen species (ROS) level was estimated through fluorescence assay. The mRNA and protein expression of Caspase-3, Caspase-9, Bcl-2, and Bax were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Results The results showed that the pretreatment of VSMCs with DMY not only significantly increased cell viability, reduced intracellular ROS release, alleviated the morphological changes of apoptosis, and decreased the apoptosis rate, but also upregulated Bcl-2 expression and downregulated Caspase-3, Caspase-9, Bax expression, and ultimately attenuated the H2O2-stimulated apoptosis. Conclusion The inhibition of DMY on VSMC apoptosis may be mediated by ROS scavenging and the activation of the mitochondrial apoptotic signaling pathway.

scholarly journals Protective Effect of Astaxanthin on Liver Fibrosis through Modulation of TGF-β1 Expression and Autophagy

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Miao Shen ◽  
Kan Chen ◽  
Jie Lu ◽  
Ping Cheng ◽  
Ling Xu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Protective Effect ◽  
Energy Production ◽  
Carotenoid Pigment ◽  
Protective Mechanisms ◽  
Clinical Issue ◽  
Significant Protective Effect ◽  
Tgf Β1

Liver fibrosis is a common pathway leading to cirrhosis and a worldwide clinical issue. Astaxanthin is a red carotenoid pigment with antioxidant, anticancer, and anti-inflammatory properties. The aim of this study was to investigate the effect of astaxanthin on liver fibrosis and its potential protective mechanisms. Liver fibrosis was induced in a mouse model using CCL4 (intraperitoneal injection, three times a week for 8 weeks), and astaxanthin was administered everyday at three doses (20, 40, and 80 mg/kg). Pathological results indicated that astaxanthin significantly improved the pathological lesions of liver fibrosis. The levels of alanine aminotransferase aspartate aminotransferase and hydroxyproline were also significantly decreased by astaxanthin. The same results were confirmed in bile duct liagtion, (BDL) model. In addition, astaxanthin inhibited hepatic stellate cells (HSCs) activation and formation of extracellular matrix (ECM) by decreasing the expression of NF-κB and TGF-β1 and maintaining the balance between MMP2 and TIMP1. In addition, astaxanthin reduced energy production in HSCs by downregulating the level of autophagy. These results were simultaneously confirmed in vivo and in vitro. In conclusion, our study showed that 80 mg/kg astaxanthin had a significant protective effect on liver fibrosis by suppressing multiple profibrogenic factors.

scholarly journals Resveratrol against 6-OHDA-induced damage of PC12 cells via PI3K/Akt

2021 ◽  
Vol 12 (1) ◽  
pp. 138-144
Author(s):  
Nanqu Huang ◽  
Juan Huang ◽  
Ying Zhang ◽  
Mingji Chen ◽  
Jingshan Shi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Akt Signaling ◽  
Leakage Rate ◽  
Motor Dysfunction ◽  
Akt Signaling Pathway ◽  
Sod Activity

Abstract Objective Our previous in vivo study found that resveratrol (Res), which is a phytoalexin, attenuated 6-hydroxydopamine (6-OHDA)-induced motor dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in rats. Therefore, we further explored the protective effect of Res on 6-OHDA-induced damage to PC12 cells in vitro with respect to the PI3K/Akt signaling pathway. Methods We incubated PC12 cells with 75 μM 6-OHDA for 24 h, and Res was then added at a final concentration of 25 μM; the protective effect was examined via MTT and lactate dehydrogenase (LDH) assays. In addition, the PI3K inhibitor LY294002 was used to investigate the potential mechanism. JC-1 staining was used to detect the mitochondrial membrane potential (MMP), and western blotting (WB) was used to detect the phosphorylation of Akt-Ser473. Results Compared with that in the control, the cell viability, total superoxide dismutase (SOD) activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly decreased, while the leakage rate of LDH was increased. And after treatment with 25 μM Res, the cell viability, total SOD activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly increased compared with those of the control cells, while the leakage rate of LDH was decreased. These effects of Res were antagonized by LY294002. Conclusions Res ameliorates 6-OHDA-induced damage to PC12 cells via activation of the PI3K/Akt signaling pathway.

scholarly journals Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

2018 ◽  
Vol 46 (5) ◽  
pp. 1793-1806 ◽  
Author(s):  
Dong-Mei Wu ◽  
Xin-Rui Han ◽  
Xin Wen ◽  
Shan Wang ◽  
Shao-Hua Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Protein Levels ◽  
Licl Treatment ◽  
Gsk 3Β

Background/Aims: Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease, and recent studies suggested that oxidative stress (OS) contributes to the cascade that leads to dopamine cell degeneration in PD. In this study, we hypothesized that salidroside (SDS) offers protection against OS injury in 6-hydroxydopamine (6-OHDA) unilaterally lesioned rats as well as the underlying mechanism. Methods: SDS and LiCl (activators of the Wnt/β-catenin signaling pathway) administration alone and in combination with 6-OHDA injection in rats was performed 3 days before modeling for 17 consecutive days to verify the regulatory mechanism by which SDS affects the Wnt/β-catenin signaling pathway as well as to evaluate the protective effect of SDS on PD in relation to OS in vivo. In addition, pheochromocytoma 12 (PC12) cells were incubated with 10 µmol/L SDS or LiCl alone or with both in combination for 1 h followed by a 24-h incubation with 100 µmol/L 6-OHDA to obtain in vitro data. Results: In vivo the administration of LiCl was found to ameliorate behavioral deficits and dopaminergic neuron loss; increase superoxide dismutase (SOA) activity, glutathione peroxidase (GSH-Px) levels, and glycogen synthase kinase 3β phosphorylation (GSK-3β-Ser9); reduce malondialdehyde (MDA) accumulation in the striatum and the GSK-3β mRNA level; as well as elevate β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-injected rats. This SDS treatment regimen was found to strengthen the beneficial effect of LiCl on 6-OHDA-injected rats. In vitro LiCl treatment decreased the toxicity of 6-OHDA on PC12 cells and prevented apoptosis. Additionally, LiCl treatment increased SOA activity, GSH-Px levels, and GSK-3β-Ser9 phosphorylation; decreased MDA accumulation in the striatum and GSK-3β mRNA levels; as well as increased β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-treated PC12 cells. Additionally, SDS treatment increased the protective effect of LiCl on 6-OHDA-treated PC12 cells. Conclusion: Evidence from experimental models suggested that SDS may confer neuroprotection against the neurotoxicity of 6-OHDA in response to OS injury and showed that these beneficial effects may be related to regulation of the Wnt/β-catenin signaling pathway. Therefore, SDS might be a potential therapeutic agent for treating PD.

scholarly journals The clinical impact of serum sLOX-1 level in coronary artery disease patients as inferred from its implication in the in vitro protective effects of metoprolol against hypoxic injury of HUVECs

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M.S Ali Sheikh ◽  
A Alduraywish ◽  
A Almaeen ◽  
U Salma ◽  
L Fei ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Protective Effect ◽  
Serum Levels ◽  
Hypoxic Injury ◽  
Injury Model ◽  
Artery Disease ◽  
Healthy Participants

Abstract Background Ischemic coronary artery disease (CAD) is a major public health problem across the world. Early detection and appropriate management significantly reduced CAD-induced morbidities and death. Endothelial cells are pathogenically implicated. Purpose Our study was designed to investigate the role of the soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) in the in vitro protective effect of Metoprolol against hypoxia-induced injury of Human umbilical vein endothelial cells (HUVECs). Secondly, the clinical significance of variations in serum levels of sLOX-1 in patients with CAD was assessed. Methods In vitro, hypoxic injury model of HUVECs was established in an atmosphere of 1% O2, 95% N2, and 5% CO2 for 24 hours. The protective effect and mechanism of action of the cardio-selective beta-blocker Metoprolol at 10–6 μM concentration was investigated. Consented stable atherosclerotic CAD (n=150) and unstable angina pectoris patients (n=75) along with 150 healthy volunteer subjects were voluntarily enrolled in this ethically approved study. Invasive coronary angiogram with ≥50% stenosis at least in one major coronary artery was used for diagnosis. ESC/ACC/AHC/practical protocols were used for categorizing patients into stable or unstable CAD. Serum sLOX-1 level was measured using specific ELISA kit. The diagnostic significance of serum sLOX-1 levels was assessed by analyzing its area under the curve (AUC). Results In vitro hypoxic conditions induced high rate of cellular apoptosis, high levels of LOX-1 expression, reactive oxygen species (ROS) generation and LDH release from HUVECs after 24 hours incubation, compared to normoxic control cells. Metoprolol significantly decreased LOX-1 levels, and prevented the release of LDH and generation of ROS. This culminated into marked improvement in cellular viability of hypoxia-exposed HUVECs (p<0.001). Compared to healthy subjects, serum levels of sLOX-1s were significantly elevated in atherosclerotic stable and unstable CAD patients (p<0.001). Serum sLOX-1 levels were increased by 4.21 folds in stable CAD patients and by 6.373 folds in atherosclerotic unstable angina patients vs. healthy participants. Moreover, the levels in the two patients' groups were significantly different (p<0.001). In stable angina CAD patients, sLOX-1 AUC = 0.929; and in unstable CAD patients, AUC = 0.944, indicating that serum sLOX-1 levels clearly differentiated patients from healthy participants with high specificity and sensitivity. Conclusions Extrapolated from HUVECs hypoxia-induced injury model and the protective effect of Metoprolol, elevation of the circulating levels of sLOX-1 correlated with increased risks for atherosclerotic CAD and is a highly sensitive and specific biomarker for early detection of the disease. Funding Acknowledgement Type of funding source: None

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