Effect of Myocardial Ischemic Reperfusion Injury on Lysosomal Enzymes and Electrolytes Content of Perfusate and Cardiac Tissue under the Influence of Desmodium gangeticum L.: An In-vitro Study

2011 ◽  
Vol 8 (1) ◽  
pp. 46-52 ◽  
Author(s):  
M. Mohamed Sh ◽  
L. Upadhyay
Keyword(s):  
Reperfusion Injury ◽  
Lysosomal Enzymes ◽  
Cardiac Tissue ◽  
In Vitro Study ◽  
Vitro Study ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Cell laden hydrogel construct on-a-chip for mimicry of cardiac tissue in-vitro study

2017 ◽  
Vol 484 (2) ◽  
pp. 225-230 ◽  
Author(s):  
Ali Ghiaseddin ◽  
Hossein Pouri ◽  
Masoud Soleimani ◽  
Ebrahim Vasheghani-Farahani ◽  
Hossein Ahmadi Tafti ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
In Vitro Study ◽  
Vitro Study

scholarly journals Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Lin Du ◽  
Jie Chen ◽  
Yong Wu ◽  
Guangwei Xia ◽  
Mingxing Chen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Protective Factor ◽  
Transforming Growth Factor ◽  
H9c2 Cell ◽  
Cerebral Stroke ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Long non-coding RNAs (lncRNAs) have been shown to play critical roles in various cell biological processes. However, the mechanism of lncRNAs in acute myocardial infarction (AMI) is not fully understood. Previous studies showed that lncRNA N1LR was down-regulated in ischemic cerebral stroke and its up-regulation was protective. The current study was designed to assess the protective effect of N1LR and further to explore potential mechanisms of N1LR in ischemic/reperfusion (I/R) injury after AMI. Male C57BL/6J mice and H9c2 cardiomyocytes were selected to construct in vivo and in vitro pathological models. In H9c2 cell line, N1LR expression was markedly decreased after H2O2 and CoCl2 treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H2O2 and CoCl2. Mouse in vivo study showed that overexpression of N1LR enhanced cardiac function and suppressed inflammatory response and fibrosis. Mechanistically, we found that the expression of transforming growth factor (TGF)-β1 and smads were significantly decreased in the N1LR overexpression group exposed to H2O2. In a summary, our study indicated that N1LR can act as a protective factor against cardiac ischemic-reperfusion injury through regulating the TGF-β/Smads signaling pathway.

scholarly journals Klotho Reduces Necroptosis by Targeting Oxidative Stress Involved in Renal Ischemic-Reperfusion Injury

2018 ◽  
Vol 45 (6) ◽  
pp. 2268-2282 ◽  
Author(s):  
Yingying Qian ◽  
Xiangjiang Guo ◽  
Lin Che ◽  
Xuejing Guan ◽  
Bei Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Tunel Staining ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

Background/Aims: Klotho is a multifunctional protein expressed predominantly in kidney tubular epithelium. Here, we investigated the protective effects of Klotho on necroptosis in renal ischemic-reperfusion injury (IRI) and the role of oxidative stress in this process. Methods: Mice were subjected to bilateral renal pedicle clamping. Mouse renal tubular epithelial (TCMK-1) cells were exposed to hypoxia/reoxygenation (H/R) or H2O2. Kidney samples from acute kidney injury (AKI) patients and controls were examined by immunofluorescence. Klotho protein and N-acetyl-L-cysteine (NAC) were used to define their roles in mediating necroptosis. Necroptosis was assessed by TUNEL staining, immunoblotting, and real-time PCR. Oxidative stress was studied via ELISA, immunoblotting, colorimetric, and thiobarbituric acid reactive substances assays. Results: Renal IRI induced Klotho deficiency in the serum and kidney, but an increase in the urine. The levels of the necroptotic markers receptor-interacting protein kinase (RIP) 1, RIP3, IL-1β, and TUNEL-positive cells increased after IRI; all increases were ameliorated by Klotho. In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2. Moreover, Klotho decreased the levels of oxidative stress biomarkers and elevated superoxide dismutase 2 expression in both in vivo and in vitro experiments. Studies in human samples further confirmed the Klotho deficiency and increased formation of RIP3 puncta in AKI kidneys. Conclusion: Klotho protects tubular epithelial cells from IRI and its anti-necroptotic role may be associated with oxidative stress inhibition.

In Vitro Study of Electroactive Tetraaniline-Containing Thermosensitive Hydrogels for Cardiac Tissue Engineering

2014 ◽  
Vol 15 (4) ◽  
pp. 1115-1123 ◽  
Author(s):  
Haitao Cui ◽  
Yadong Liu ◽  
Yilong Cheng ◽  
Zhe Zhang ◽  
Peibiao Zhang ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cardiac Tissue ◽  
In Vitro Study ◽  
Cardiac Tissue Engineering ◽  
Vitro Study ◽  
Thermosensitive Hydrogels

scholarly journals Dihydromyricetin Ameliorates Cardiac Ischemia/Reperfusion Injury through Sirt3 Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Liping Wei ◽  
Xuseng Sun ◽  
Xin Qi ◽  
Yufan Zhang ◽  
Yuanyang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
In Vitro Study ◽  
Vitro Study ◽  
Ampelopsis Grossedentata

During myocardial infarction, quickly opening the occluded coronary artery is a major method to save the ischemic myocardium. However, it also induces reperfusion injury, resulting in a poor prognosis. Alleviating the reperfusion injury improves the prognosis of the patients. Dihydromyricetin (DHM), a major component in the Ampelopsis grossedentata, has numerous biological functions. This study aims to clarify the effects of DHM under the ischemia/reperfusion (I/R) condition. We elucidated the role of Sirt3 in the cardiomyocyte response to DHM based on the hearts and primary cardiomyocytes. Cardiac function, mitochondrial biogenesis, and infarct areas were examined in the different groups. We performed Western blotting to detect protein expression levels after treatments. In an in vitro study, primary cardiomyocytes were treated with Hypoxia/Reoxygenation (H/R) to simulate the I/R. DHM reduced the infarct area and improved cardiac function. Furthermore, mitochondrial dysfunction was alleviated after DHM treatment. Moreover, DHM alleviated oxidative stress indicated by decreased ROS and MnSOD. However, the beneficial function of DHM was abolished after removing the Sirt3. On the other hand, the mitochondrial function was improved after DHM intervention in vitro study. Interestingly, Sirt3 downregulation inhibited the beneficial function of DHM. Therefore, the advantages of DHM are involved in the improvement of mitochondrial function and decreased oxidative stress through the upregulation of Sirt3. DHM offers a promising therapeutic avenue for better outcome in the patients with cardiac I/R injury.

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