The Protective Effect of Stichopus japonicus Fucoidan on PC12 Cells with Hypoxia/Reoxygenation Injury

2014 ◽  
Vol 556-562 ◽  
pp. 610-614
Author(s):  
Shu Liang Song ◽  
Wei Wang ◽  
Xiao Chen Wang ◽  
Hao Liang ◽  
Yun Shan Wang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Apoptotic Pathway ◽  
Apoptosis Pathway ◽  
Stichopus Japonicus ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

In this study the effect of fucoidan SJP-3 extracted from Stichopus Japonicus was used to evaluate the protective effect on PC12 cells with hypoxia/reoxygenation injury. SJP-3 can stabilize the mitochondrial membrane potential and resistant Cyt-C/mitochondrial apoptotic pathway via increasing the Bcl-2 expression and decreasing expression of the Bax, caspase-3, caspase-9 suggesting that SJP-3 may exert a protective effects on neural cells with hypoxia/reoxygenation injury through the protection of mitochondria, the stability of mitochondrial membrane potential and inhibition of mitochondrial apoptosis pathway.

scholarly journals Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Vu Thi Thu ◽  
Ngo Thi Hai Yen
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cell Group ◽  
H9c2 Cell ◽  
H9c2 Cells ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

This study was conducted to evaluate the protective effect of Naringin (NAR) on H9C2 cardiomyocytes in hypoxia/reoxygenation (HR) injury in vitro induced by the hypoxia chamber. Methods: H9C2 cells were grown under normal (control) and HR conditions. The viability, cardiolipin content and mitochondrial membrane potential of H9C2 cells in experimental groups were analyzed by using suitable kits. Results: The obtained results showed that the addition of Naringin (16÷160 µM) significantly increased the survival rate of H9C2 cells under HR conditions. In particular, NAR had the highest efficiency in preserving mitochondrial function at concentrations of 80 µM and 160 µM. In HR-exposed H9C2 cell group, the cardiolipin content and mitochondrial membrane potential values of H9C2 cells were decreased sharply with that of control (71,64±1,37% and 68,12±2,78%, p<0,05). Interestingly, mitochondrial cardiolipin contents were signigicantly increased in H9C2 cells post-hypoxic treated wtih NAR at dose of 80 µM 160 µM to 87,76±1,89% and 81,09±1,21%. Additionally, post-hypoxic supplementation of NAR at concentration of 80 µM and 160 µM effectively increased mitochondrial membrane potential values. Conclusion: The obtained results are preliminary data on the effects of NAR in protecting mitochondrial-targeted cardiomyocytes against HR injury.

scholarly journals Sevoflurane Postconditioning Attenuates Hypoxia/Reoxygenation Injury of Cardiomyocytes Under High Glucose by Regulating HIF-1α/MIF/AMPK Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Haiping Ma ◽  
Yongjie Li ◽  
Tianliang Hou ◽  
Jing Li ◽  
Long Yang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Cell Viability ◽  
Mrna Expression ◽  
High Glucose ◽  
Mitochondrial Membrane ◽  
Ampk Signaling ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

Subject: Cardiovascular disease, as a very common and serious coexisting disease in diabetic patients, and is one of the risk factors that seriously affect the prognosis and complications of surgical patients. Previous studies have shown that sevoflurane post-conditioning (SPostC) exerts a protective effect against myocardial ischemia/reperfusion injury by HIF-1α, but the protective effect is weakened or even disappeared under hyperglycemia. This study aims to explore whether regulating the HIF-1α/MIF/AMPK signaling pathway can restore the protective effect and reveal the mechanism of SPostC on cardiomyocyte hypoxia/reoxygenation injury under high glucose conditions.Methods: H9c2 cardiomyocytes were cultured in normal and high-concentration glucose medium to establish a hypoxia/reoxygenation (H/R) injury model of cardiomyocytes. SPostC was performed with 2.4% sevoflurane for 15 min before reoxygenation. Cell damage was determined by measuring cell viability, lactate dehydrogenase activity, and apoptosis; Testing cell energy metabolism by detecting reactive oxygen species (ROS) generation, ATP content and mitochondrial membrane potential; Analysis of the change of HIF-1α, MIF and AMPKα mRNA expression by RT-PCR. Western blotting was used to examine the expression of HIF-1α, MIF, AMPKα and p-AMPKα proteins. HIF-1α and MIF inhibitors and agonists were administered 40 min before hypoxia.Results: 1) SPostC exerts a protective effect by increasing cell viability, reducing LDH levels and cell apoptosis under low glucose (5 μM) after undergoing H/R injury; 2) High glucose concentration (35 μM) eliminated the cardioprotective effect of SPostC, which is manifested by a significantly decrease in the protein and mRNA expression level of the HIF-1α/MIF/AMPK signaling pathway, accompanied by decreased cell viability, increased LDH levels and apoptosis, increased ROS production, decreased ATP synthesis, and decreased mitochondrial membrane potential; 3. Under high glucose (35 μM), the expression levels of HIF-1α and MIF were up-regulated by using agonists, which can significantly increase the level of p-AMPKα protein, and the cardioprotective effect of SPostC was restored.Conclusion: The signal pathway of HIF-1α/MIF/AMPK of H9c2 cardiomyocytes may be the key point of SPostC against H/R injure. The cardioprotective of SPostC could be restored by upregulating the protein expression of HIF-1α and MIF under hyperglycemia.

scholarly journals p38-mediated Regulation of an Fas-associated Death Domain Protein-independent Pathway Leading to Caspase-8 Activation during TGFβ-induced Apoptosis in Human Burkitt Lymphoma B Cells BL41

2001 ◽  
Vol 12 (10) ◽  
pp. 3139-3151 ◽  
Author(s):  
Nicolas Schrantz ◽  
Marie-Françoise Bourgeade ◽  
Shahul Mouhamad ◽  
Gérald Leca ◽  
Surendra Sharma ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Transforming Growth Factor ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Caspase 8 ◽  
Death Domain ◽  
Apoptotic Pathway ◽  
Domain Protein

On binding to its receptor, transforming growth factor β (TGFβ) induces apoptosis in a variety of cells, including human B lymphocytes. We have previously reported that TGFβ-mediated apoptosis is caspase-dependent and associated with activation of caspase-3. We show here that caspase-8 inhibitors strongly decrease TGFβ-mediated apoptosis in BL41 Burkitt's lymphoma cells. These inhibitors act upstream of the mitochondria because they inhibited the loss of mitochondrial membrane potential observed in TGFβ-treated cells. TGFβ induced caspase-8 activation in these cells as shown by the cleavage of specific substrates, including Bid, and the appearance of cleaved fragments of caspase-8. Our data show that TGFβ induces an apoptotic pathway involving sequential caspase-8 activation, loss of mitochondrial membrane potential, and caspase-9 and -3 activation. Caspase-8 activation was Fas-associated death domain protein (FADD)-independent because cells expressing a dominant negative mutant of FADD were still sensitive to TGFβ-induced caspase-8 activation and apoptosis. This FADD-independent pathway of caspase-8 activation is regulated by p38. Indeed, TGFβ-induced activation of p38 and two different inhibitors specific for this mitogen-activated protein kinase pathway (SB203580 and PD169316) prevented TGFβ-mediated caspase-8 activation as well as the loss of mitochondrial membrane potential and apoptosis. Overall, our data show that p38 activation by TGFβ induced an apoptotic pathway via FADD-independent activation of caspase-8.

Protective effect of the dimer of 16,16-diMePGB1 against KCN-induced mitochondrial failure in hepatocytes

1992 ◽  
Vol 263 (2) ◽  
pp. C405-C411 ◽  
Author(s):  
Y. Park ◽  
T. M. Devlin ◽  
D. P. Jones
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Ion Transport ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Time Dependent ◽  
Dependent Manner ◽  
Protective Effects ◽  
Cellular Swelling

The dimer and trimer of 16,16-dimethyl-15-dehydroprostaglandin B1 (16,16-diMePGB1) previously have been shown to have protective effects on mitochondrial function. To examine the potential mechanisms involved in protection against mitochondrial failure, we have studied the effects of the dimer of 16,16-diMe-PGB1 (dicalciphor) on mitochondrial function in hepatocytes exposed to KCN. Addition of micromolar concentrations of dicalciphor provided substantial protection against KCN-induced toxicity in a concentration- and time-dependent manner. Dicalciphor, however, had no effect on total or mitochondrial ATP losses in KCN-treated cells. The dimer prevented the marked loss of mitochondrial membrane potential (delta psi) and delta pH that occurs as a result of KCN treatment and prevented KCN-induced loading of phosphate in mitochondria. Furthermore, the dimer of 16,16-diMePGB1 also prevented KCN-induced mitochondrial and cellular swelling. These results demonstrate that dicalciphor protects against KCN-induced damage and that this protection is associated with regulation of specific mitochondrial ion transport functions.

Assessment of mitochondrial membrane potential in proximal tubules after hypoxia-reoxygenation

2005 ◽  
Vol 288 (6) ◽  
pp. F1092-F1102 ◽  
Author(s):  
Thorsten Feldkamp ◽  
Andreas Kribben ◽  
Joel M. Weinberg
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Atp Hydrolysis ◽  
Proximal Tubules ◽  
Green Fluorescence ◽  
Direct Assessment ◽  
Dynamic Studies ◽  
Safranin O ◽  
Hypoxia Reoxygenation

Proximal tubules develop a severe energetic deficit during hypoxia-reoxygenation (H/R) that previous studies using fluorescent potentiometric probes have suggested is characterized by sustained, partial mitochondrial deenergization. To validate the primary occurrence of mitochondrial deenergization in the process, optimize approaches for estimating changes in mitochondrial membrane potential (ΔΨm) in the system, and clarify the mechanisms for the defect, we further investigated the behavior of 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazocarbocyanine iodide (JC-1) in these cells and introduce a more dynamic and quantitative approach employing safranin O for use with the tubule system. Although use of JC-1 can be complicated by decreases in the plasma membrane potential that limit cellular uptake of JC-1 and such behavior was demonstrated in ouabain-treated tubules, changes in ΔΨm entirely accounted for the decreases in the formation of red fluorescent JC-1 aggregates and in the ratio of red/green fluorescence observed after H/R. The red JC-1 aggregates did not readily dissociate when tubules were deenergized after JC-1 uptake, making it unsuitable for dynamic studies of energization. Safranin O uptake by digitonin-permeabilized tubules required very small numbers of tubules, permitted measurements of ΔΨm for relatively prolonged periods after the end of the experimental maneuvers, was rapidly reversible during deenergization, and allowed for direct assessment of both substrate-dependent, electron transport-mediated ΔΨm, and ATP hydrolysis-supported ΔΨm. Both types of energization measured using safranin O in tubules permeabilized after H/R were impaired, but combining substrates and ATP substantially restored ΔΨm.

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