Protective Effect of Isoflurane on Myocardial Ischemia-Reperfusion Injury in Rats Through P38MAPK Signaling Pathway

2020 ◽  
Vol 10 (8) ◽  
pp. 1225-1230
Author(s):  
Zheng Liu ◽  
Mingming Zhang ◽  
Mangyuan Wang ◽  
Tao Zhu ◽  
Qiang Huo
Keyword(s):  
P38 Mapk ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Apoptosis ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Group I ◽  
P38mapk Signaling ◽  
Mda Content

Objective: Abnormal p38 MAPK activation involves in ischemia-reperfusion (IR) injury. Isoflurane (ISO) is a clinically used inhaled anesthetic and protects myocardial I-R injury. Our study assessed whether ISO exerts a protective role in myocardial I-R injury. Methods: Rat myocardial I-R injury model was set followed by analysis of p-p38 MAPK expression in myocardial tissue by western blot, caspase-3 activity, as well as MDA and SOD content. Rats were assigned into Sham group, IR group, I-R + ISO group, followed by measuring p-p38 MAPK expression, caspase-3 activity, MDA and SOD, cell apoptosis and ROS content. Results: Compared with Sham group, MDA content, caspase-3 activity and p-p38 MAPK protein expression as well as ROS content and apoptosis rate in I-R model rats were significantly increased and SOD activity was significantly decreased. ISO pretreatment significantly reduced MDA content, caspase-3 activity, ROS content and apoptosis rate in I-R model rats, increased SOD activity and reduced p-p38 MAPK expression. Conclusion: Activation of p38MAPK signaling plays a role in mediating myocardial IR injury and cardiomyocyte apoptosis. ISO pretreatment inhibits oxidative stress and cardiomyocyte apoptosis and protects myocardial IR injury via inhibiting p38MAPK signaling.

Analyzing the anti-ischemia–reperfusion injury effects of ginsenoside Rb1 mediated through the inhibition of p38α MAPK

2016 ◽  
Vol 94 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Gonghao Li ◽  
Wenhao Qian ◽  
Changyun Zhao
Keyword(s):  
P38 Mapk ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinase ◽  
Ginsenoside Rb1 ◽  
Group I ◽  
Tnf Α ◽  
P38α Mapk

Recent studies have demonstrated that ginsenoside Rb1 protects the myocardium from ischemia–reperfusion (I/R) injury. However, the precise mechanisms for this protection have not been determined. This study aimed to determine whether the attenuation of I/R-induced myocardial injury by ginsenoside Rb1 (GS Rb1) is due to inhibition of p38α mitogen-activated protein kinase (MAPK). Sprague–Dawley rats were distributed among 6 treatment groups: sham group; I/R group; p38 MAPK inhibitor SB203580 group (SB + I/R); GS Rb1 group (GS + I/R); p38 MAPK agonist anisomycin group (Ani + I/R); and the GS Rb1 + Ani group (GS + Ani + I/R). All of the anaesthetized rats, except those in the sham group, underwent an open-chest procedure that involved 30 min of myocardial ischemia followed by 2 h of reperfusion. Myocardial infarction size (MIS), caspase-3 activity, and levels of the cytokine tumor necrosis factor alpha (TNF-α) in the myocardium were monitored. The expressions of p38α MAPK, caspase-3, and TNF-α in the myocardium were assayed. GS Rb1 reduced MIS and attenuated caspase-3 activity and the levels of TNF-α in the myocardium. Protein expression of total p38α MAPK was not significantly altered. In the Ani + I/R and I/R groups, the levels of phospho-p38α MAPK were significantly increased compared with the sham group, and these increased levels were reduced with GS Rb1. Hemodynamic parameters were not significantly different between the GS + I/R and SB + I/R groups. GS Rb1 exerts an anti-apoptotic effect that protects against I/R injury by inhibiting p38α MAPK phosphorylation, suggesting that GS Rb1-mediated protection requires the inhibition of p38α MAPK.

Rehmanniae Decoction Improve Brain Function in Vascular Dementia Rats Through Phosphoinositide 3-Kinase (PI3K)/AKT Signaling Pathway

2020 ◽  
Vol 10 (4) ◽  
pp. 538-544
Author(s):  
Peng Sang ◽  
Jiahui Zhao ◽  
Shun Wang ◽  
Hui Yang ◽  
Huijuan Shi
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Sham Group ◽  
Akt Signaling ◽  
Sod Activity ◽  
Memory Ability ◽  
Group I ◽  
Mda Content

Objective: Studies have shown that Rehmanniae Decoction (Reh) has therapeutic effect on vascular dementia (VD). PI3K/AKT signaling regulates oxidative stress damage and cell apoptosis. Our study intends torehmanniae decoction's effect on the neural function in VD mice. Methods: The mice were divided into Sham group, VD group, low dose Reh+ VD group and high dose Reh+ VD group. Water maze test was used to assess learning and memory ability. The activity of caspase-3, the content of MDA and the activity of SOD enzyme in hippocampus were detected. In vitro , HT22 cells were divided into control group, I–R group, I–R+ 2% Reh serum, I–R+ 4% Reh serum. Flow cytometry was used to detect the intracellular content of ROS and cell apoptosis. Results: Compared with sham group, the learning and memory ability of mice in VD group was significantly decreased. p-AKT level and SOD activity in the hippocampus was decreased, the Caspase-3 activity and MDA content was significantly increased. After treatment of Reh, the learning and memory ability of VD model mice was significantly improved, p-AKT protein expression and SOD activity were up-regulated, and Caspase-3 activity and MDA content were reduced. Conclusion: Rehmanniae decoction alleviates the oxidative stress and inhibits cell apoptosis to improve the function of brain by regulating PI3K/AKT pathway.

scholarly journals The expression and role of β3AR protein in myocardial ischemia/reperfusion in rats

2021 ◽  
Author(s):  
Zi-Long Wang ◽  
Xiao-Chen Sun ◽  
Rong Luo ◽  
Dong-Ye Li ◽  
Hao-Chen Xuan
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Sd Rats ◽  
Group I ◽  
Myocardial Ischemia Reperfusion

IntroductionTo explore serum norepinephrine (NE) concentration and β3-adrenoceptor (β3AR) protein expression at different times during myocardial ischemia/reperfusion (I/R) and examine the role of β3AR in I/R.Material and methods28 Sprague-Dawley (SD) rats were randomly divided into one sham group and six I/R groups. The rats in the I/R groups were subjected to ischemia for 45 minutes. After reperfusion, the serum NE concentration and the β3AR protein expression in the myocardial tissue of the left ventricular injury region were detected. Another 18 SD rats were randomly divided into a sham group, I/R groups, and I/R + BRL37344 group.ResultsCompared with the sham group, the serum NE concentration of rats in the I/R groups significantly increased at 6 hours (P < 0.001). The serum NE concentration and myocardial β3AR protein expression were both highest at 72 hours. Compared with the sham group, the expressions of the pro-apoptotic proteins Bax and cleaved caspase-3 after I/R were significantly increased (P < 0.01, P < 0.001, respectively), and the expression of anti-apoptotic protein Bcl-2 was significantly decreased (P < 0.01). Compared with I/R groups, the expressions of Bax and cleaved caspase-3 in the I/R + BRL37344 group were significantly decreased (P < 0.05, P < 0.01, respectively).ConclusionsWith the prolongation of myocardial I/R in rats, serum NE concentration and β3AR protein expression showed a significant increase trend and reached a peak at 72 hours. Specific β3AR agonist BRL37344 can reduce myocardial I/R injury in vivo in rats, alleviate apoptosis, reduce infarct size, and improve cardiac function.

Paricalcitol pretreatment attenuates renal ischemia/reperfusion injury by inhibiting p38 MAPK and activating PI3K/Akt signaling pathways

2019 ◽  
Vol 44 (4) ◽  
pp. 452-461
Author(s):  
Zahide Cavdar ◽  
Cemre Ural ◽  
Ayse Kocak ◽  
Sevki Arslan ◽  
Sibel Ersan ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Albino Rats ◽  
Sod Activity ◽  
Interstitial Inflammation ◽  
Tnf Α ◽  
Active Caspase

Abstract Objective This study aimed to investigate the renoprotective effects of paricalcitol, a synhetic vitamin D analog, through its possible roles on p38 MAPK and PI3K/Akt signaling pathways to prevent oxidative stress, inflammation and apoptosis during renal I/R. Materials and methods Total 20 kidney tissues of sham (n = 6), subjected to renal I/R bilaterally for 45 min ischemia followed by 24 h reperfusion (n = 7) and paricalcitol (0.3 μg/kg, ip) pretreated Wistar albino rats (n =7) were used in this study. Interstitial inflammation and active caspase-3 expression were evaluated histologically. TNF-α, IL-1β, kidney injury molecule-1 (KIM-1), MDA and SOD activity in kidneys were analysed biochemically. Furthermore, activation of p38 MAPK, PI3K/Akt signaling pathways and NFκB p65 were evaluated by western blot. Results Paricalcitol pretreatment significantly reduced interstitial inflammation during renal I/R, which was consistent with decreased tumor TNF-α, IL-1β, active caspase-3 and KIM-1 expression. Paricalcitol also reduced MDA level and attenuated the reduction of SOD activity in the kidney during I/R. Moreover, paricalcitol could suppress the p38 MAPK and NFκB p65, and also activate PI3K/Akt signaling pathway during renal I/R. Conclusion All these findings indicate that paricalcitol may be an effective practical strategy to prevent renal I/R injury.

Sufentanil Affects High Glucose-Induced Oxidative Stress in and Apoptosis of Cardiomyocytes by Regulation of miR-142-3p Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 466-470
Author(s):  
Zhiyong Liu ◽  
Cuiqing Ding ◽  
Changqing Yao ◽  
Jinhui Chen
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content

To explore the effects and molecular mechanisms of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes, cardiomyocytes H9c2 cells were classified into groups based on different treatments as high-glucose (HG), HG with low, medium, or high-dose sufentanil, HG with high-dose sufentanil and anti-miR-NC, HG with high-dose sufentanil and anti-miR-142-3p, and control. The cells’ superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using respective kits. The apoptosis rate in each group was detected by flow cytometry. The expressions of cleaved caspase-3 and pro-caspase3 were determined using western blotting. The expression of miR-142-3p in cardiomyocytes was detected using real-time fluorescent quantitative PCR. Compared with the control group, the HG group had decreased SOD activity, pro-caspase-3 expression, and miR-142-3p expression and increased MDA content, apoptosis, and cleaved caspase-3 expression (P < 0.05). Compared with the HG group, the SOD activity and pro-caspase-3 expression increased and the MDA content, apoptosis rate, and cleaved caspase-3 expression decreased in HG cells treated with low, medium, or high-dose sufentanil. The expression of miR-142-3p was increased in a dose-dependent manner (P < 0.05). The interference of miR-142-3p reversed the effect of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes. Sufentanil may inhibit high glucose-induced oxidative stress in and apoptosis of cardiomyocytes by upregulating miR-142-3p expression.

scholarly journals Inactivated Lactobacillus promotes protection against myocardial ischemia–reperfusion injury through NF-κB pathway

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Ni Wang ◽  
Genhong Song ◽  
Yang Yang ◽  
Weiwei Yuan ◽  
Ming Qi
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Group Model ◽  
Content Increase ◽  
Model Group ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content ◽  
Myocardial Ischemia Reperfusion

Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion may augment tissue injury in excess of that produced by ischemia alone. So this experiment was designed to study the protective effects and mechanism of inactivated Lactobacillus (Lac) on myocardial ischemia–reperfusion (I–R) injury (MIRI). MIRI rat models were established by ligation of left anterior descending coronary artery for ~30 min and then, reperfusion for 120 min and divided into control group, model group, and Lac (106, 107, and 108 cfu/kg) groups. At the end of the test, the creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assayed by corresponding kits. The heart was obtained from rats and the myocardial infarction area was determined by TTC staining and myocardial endothelial cell apoptosis rate was determined by Tunel kit. Besides, A20, IκB, nuclear factor (NF)-κB, and nitric oxide (NO) synthase (NOS) were also assayed by Western blot. When compared with model group, Lac obviously reduces MIRI in the rat by reducing myocardial infarction area and the apoptosis rate of endothelial cells; reduce the serum CK, LDH, and MDA content; increase the serum SOD activity; and suppress NF-κB signaling and NOS expression in the myocardial tissues. Lac pretreatment can inhibit lipid peroxidation and effectively improve MIRI caused by oxygen free radical through inhibiting NF-κB signaling.

Resveratrol Reduces Cardiomyocyte Apoptosis Induced by I-R Injury Through Upregulating DJ-1

2020 ◽  
Vol 10 (12) ◽  
pp. 1786-1792
Author(s):  
Xiaoyan Wu ◽  
Zengfan Wu
Keyword(s):  
Cell Apoptosis ◽  
Caspase 3 ◽  
Control Group ◽  
Related Factor ◽  
Ros Production ◽  
H9c2 Cells ◽  
Sod Activity ◽  
Nrf2 Pathway ◽  
Group I ◽  
Mda Content

The NF-E2 related factor 2 (Nrf2) involves in anti-oxidative stress. DJ-1 is a multifunctional protein widely distributed in various tissues that plays a role in enhancing Nrf2 stability and promoting Nrf2 protein expression. Resveratrol (Res) is an important polyphenolic substance with various pharmacological effects, such as anti-oxidation and protection of cardiovascular and cerebrovascular. Our study intends to assess Resveratrol?s role in regulating DJ-1/Nrf2 pathway activity and alleviating rat cardiomyocyte I-R injury. Rat cardiomyocyte I-R injury model was established to detect DJ-1 and Nrf2 expressions, caspase-3 activity, malondialdehyde (MDA), and superoxide dismutase (SOD). The I-R rats were assigned into I-R group, I-R+Res 20 (20 mg/Kg) group, and I-R+Res 40 (20 mg/Kg) group. Rat H9C2 cells were assigned into control group, I-R group, and I-R+Res group followed by analysis of cell apoptosis and reactive oxygen species (ROS) by flow cytometry. The MDA content and caspase-3 activity were significantly elevated, while the SOD activity was obviously reduced in the cardiomyocyte of the I-R model rats. DJ-1 and Nrf2 expressions were apparently upregulated in I-R model. MDA content and caspase-3 activity were significantly decreased, whereas SOD activity, DJ-1, and Nrf2 expression levels were obviously elevated in Res treatment group with dose dependence. I-R treatment induced H9C2 cell apoptosis and intracellular ROS production, and upregulated DJ-1 and Nrf2 expressions. Res treatment further enhanced DJ-1 and Nrf2 levels, attenuated ROS production, and reduced apoptotic rate in H9C2 cells under I-R treatment. Res attenuates brain cell apoptosis and neuronal damage after I-R by increasing DJ-1 level, enhancing DJ-1/Nrf2 pathway, and elevating the anti-oxidation level.

Dexmedetomidine Suppressing Apoptosis to Release Rats’ Liver Ischemia-Reperfusion Injury

2021 ◽  
Vol 11 (8) ◽  
pp. 1536-1542
Author(s):  
Zhao Hai-Fan ◽  
Li Chong ◽  
Hu Zhi-Duo ◽  
Chen Hong ◽  
Jiang Tao ◽  
...  
Keyword(s):  
Western Blot ◽  
Liver Tissue ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological State ◽  
Inhibitory Effects ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Purpose: Explore the dexmedetomidine’s therapeutic impact on hepatic ischemia-reperfusion (I/R) injury and the related principle. Methods: The work established the rats’ liver I/R model. Liver tissues’ pathological state from each rat was evaluated by HE staining. ELISA was utilized to confirm the activity of MDA and SOD in the liver tissue, AST in the serum, and the ALT’s concentration. The apoptotic state of liver tissue was detected by TUNEL assay. Bcl-2, Caspase-3, HO-1, and BAX’s expressions of each rat’s liver tissue had been confirmed through immunohistochemistry and western blot. Results: Rats’ liver injury from I/R group and DEX+A group was rat’s liver tissue had been confirmed through immunohistochemistry and western blot. severer than that from Sham group in terms of HE staining and ELISA. The injured tissue has been improved by the introduction of Dexmedetomidine. The TUNEL, Immunohistochemistry and Western Blot results indicated that the high apoptotic rate in I/R model was inhibited using Dexmedetomidine. However, the inhibitory effects were reversed by the co-administration of Atipamezole. Conclusion: Dexmedetomidine suppressed apoptosis to alleviate rats’ hepatic ischemia-reperfusion injuries.

Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion

2005 ◽  
Vol 288 (1) ◽  
pp. H221-H226 ◽  
Author(s):  
Meijing Wang ◽  
Ben M. Tsai ◽  
Ajay Kher ◽  
Lauren B. Baker ◽  
G. Mathenge Wairiuko ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Functional Recovery ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Caspase 1 ◽  
Tnf Α

Myocardial ischemia is the leading cause of death in both men and women; however, very little information exists regarding the effect of testosterone on the response of myocardium to acute ischemic injury. We hypothesized that testosterone may exert deleterious effects on myocardial inflammatory cytokine production, p38 MAPK activation, apoptotic signaling, and myocardial functional recovery after acute ischemia-reperfusion (I/R). To study this, isolated, perfused rat hearts (Langendorff) from adult males, castrated males, and males treated with a testosterone receptor blocker (flutamide) were subjected to 25 min of ischemia followed by 40 min of reperfusion. Myocardial contractile function (left ventricular developed pressure, left ventricular end-diastolic pressure, positive and negative first derivative of pressure) was continuously recorded. After reperfusion, hearts were analyzed for expression of tissue TNF-α, IL-1β, and IL-6 (ELISA) and activation of p38 MAPK, caspase-1, caspase-3, caspase-11, and Bcl-2 (Western blot). All indices of postischemic myocardial functional recovery were significantly higher in castrated males or flutamide-treated males compared with untreated males. After I/R, castrated male and flutamide-treated male hearts had decreased TNF-α, IL-1β, and IL-6; decreased activated p38 MAPK; decreased caspase-1, caspase-3, and caspase-11; and increased Bcl-2 expression compared with untreated males. These results show that blocking the testosterone receptor (flutamide) or depleting testosterone (castration) in normal males improves myocardial function after I/R. These effects may be attributed to the proinflammatory and/or the proapoptotic properties of endogenous testosterone. Further understanding may allow therapeutic manipulation of sex hormone signaling mechanisms in the treatment of acute I/R.

scholarly journals Protective effects of tempol in an experimental ovarian ischemia–reperfusion injury model in female Wistar albino rats

2017 ◽  
Vol 95 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Neslihan Pınar ◽  
Oya Soylu Karapınar ◽  
Oğuzhan Özcan ◽  
Esin Atik Doğan ◽  
Suphi Bayraktar
Keyword(s):  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Index ◽  
Albino Rats ◽  
Protective Effects ◽  
Group V ◽  
Group Iii ◽  
Group I ◽  
Wistar Albino Rats

The aim of this study was to investigate the antioxidant effects of tempol on ovarian ischemia–reperfusion (I/R) injury in rats. Forty female Wistar albino rats were randomly divided into 5 groups: Group I, sham; Group II, ischemia (I); Group III, I/R; Group IV, I/R + tempol 30 mg/kg i.p; Group V, I/R + tempol 50 mg/kg i.p. Oxidative stress index (OSI) was significantly higher in the ischemia group and the I/R group than in the sham group. Catalase levels were significantly lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. Glutathione peroxidase levels were lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. MDA levels were significantly lower in the I/R + tempol 30 mg/kg i.p. group and the I/R + tempol 50 mg/kg i.p. group than in the I/R group. The levels of the histopathological parameters were significantly decreased in the I/R + tempol 50 mg/kg i.p. group compared with the I/R group. Tempol can be used for reducing ovarian I/R injury.

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