scholarly journals Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Shi Shu ◽  
Chun-Ming Li ◽  
Yan-Li You ◽  
Xiao-Lu Qian ◽  
Shuang Zhou ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Neurological Deficit ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Beclin 1 ◽  
Male Rats ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Sham Operation Group

Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed.Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats.Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis.Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h.Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia.

scholarly journals Protective Effects of Sesamol on the Brains of Rats with Focal Cerebral Ischemia-Reperfusion Injury

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Guannan X ◽  
◽  
Xiujuan G ◽  
Xin L ◽  
Yujue Z ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Reperfusion Injury ◽  
Cerebral Edema ◽  
Neurological Deficit ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cerebrovascular Event ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Stroke is an acute cerebrovascular event associated with brain tissue injury, representing the most common cause of death. Thrombolysis and recanalization are the principal treatment modalities for ischemic stroke. Some patients experience cerebral ischemia-reperfusion injury following treatment. A previous study established that sesamol is effective in reducing risk factors for stroke. Here, we aimed to investigate the protective effect of sesame phenol on cerebral ischemia-reperfusion injury. A total of 72 SD rats were randomly divided into a sham group, cerebral ischemia-reperfusion (MCAO) group, cerebral ischemia-reperfusion with low dose sesame phenol (MCAO+sesamol A) group and cerebral ischemia-reperfusion with high dose sesame phenol (MCAO + sesamol B) group. After cerebral ischemia had been induced for 2h and reperfusion conducted for 24h, the volume of cerebral infarction, the degree of cerebral edema and the neurological deficit scores were tested. The results showed sesamin improved the neurological deficit score in a dose-dependent manner, reduced the volume of cerebral infarction, degree of cerebral edema. Prophylactic treatment with sesame phenol provided neuroprotective effects on cerebral ischemia-reperfusion injury.

MicroRNA-26b-5p alleviates cerebral ischemia-reperfusion injury in rats via inhibiting the N-myc/PTEN axis by downregulating KLF10 expression

2021 ◽  
pp. 096032712199189
Author(s):  
Y Xiao ◽  
S Zheng ◽  
N Duan ◽  
X Li ◽  
J Wen
Keyword(s):  
Cell Proliferation ◽  
Cerebral Ischemia ◽  
Pc12 Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sham Operation ◽  
Inflammatory Factor ◽  
Sham Operation Group ◽  
Cerebral Ischemia Reperfusion ◽  
Factor Secretion

MicroRNAs plays important role in cerebral ischemia-reperfusion (CIR). However, the role of miR-26b-5p in CIR injury remains unclear. PC12 cells were treated with oxygen-glucose deprivation (OGD) for 0 h, 2 h, 4 h, 6 h, and then reoxygenated for 24 h to construct an in vitro I/R model. Then, miR-26b-5p mimic, small interfering RNA of KLF10 and KLF10 overexpression plasmid were transfected into cells respectively for mechanism study. Our results showed that miR-26b-5p was downregulated in OGD/R-induced PC12 cells. After overexpression of miR-26b-5p, cell proliferation ability was enhanced, apoptosis, ROS and inflammatory mediators were inhibited. Bioinformatics analysis indicated that miR-26b-5p was directly bound to the 3’ UTR of KLF10, and downregulated the expression of KLF10. KLF10 was upregulated in OGD/R cells, and transfection with si-KLF10 promoted cell proliferation and reduced apoptosis, NO concentration and inflammatory factor secretion. Moreover, pcDNA-KLF10 reversed the inhibitory effects of miR-26b-5p mimic on apoptosis, NO content and inflammatory factor secretion, as well as the downregulation of N-myc and PTEN expression. Meanwhile, I/R rat models were constructed and divided into sham operation group (femoral artery isolation only), model group (middle cerebral artery occlusion model of rats was prepared by thread embolization), treatment group (200 µL of miR-26b-5p mimic was injected into the brain of model rats). We observed that the infarct size of brain tissue was reduced, KLF10 expression was downregulated, and apoptosis and inflammatory response were reduced. These results suggest that miR-26b-5p had protective effects on CIRI and it may be a potential treatment target.

scholarly journals The Effect of Erythropoietin on Ischemia/Reperfusion Injury after Testicular Torsion/Detorsion: A Randomized Experimental Study

ISRN Urology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Fahimeh Kazemi Rashed ◽  
Babollah Ghasemi ◽  
Hamid Deldade Mogaddam ◽  
Mehran Mesgari
Keyword(s):  
Testicular Torsion ◽  
Ischemia Reperfusion Injury ◽  
Protective Efficacy ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Sham Operation ◽  
Scoring Method ◽  
Group Vi ◽  
Sham Operation Group ◽  
Group I

This study was conducted to investigate the protective effect of erythropoietin (EPO) on ischemia/reperfusion related changes after testicular torsion/detorsion. In a randomized experimental trial 30 male rats were randomly allocated into six equal groups of five rats each. Group I (orchiectomy for histopathologic examination), group II (sham operation), group III (torsion for 2 hours, and ischemia/detorsion for 24 hours, and orchiectomy); group IV (torsion for 2 hours, ischemia/detorsion for 24 hours with erythropoietin injection then orchiectomy), group V (torsion for 2 hours and detorsion and EPO injection and orchiectomy 1 week later, group VI (torsion for 2 hours/detorsion and orchiectomy 1 week later). Two groups (groups 4 and 5) received different protocols of erythropoietin administration after testicular torsion/distortion. other groups were not receiving erythropoietin. Johnsen’s spermatogenesis scoring method and Cosentino’s histologic staging method were used to assess main outcome measures of the study. After the experimentation, Johnsen’s score in EPO Groups was statistically different from the score in some groups not receiving erythropoietin. Cosentino’s score in EPO groups was statistically different from the score in all groups not receiving erythropoietin. Neovascularization, vascular necrosis, vascular congestion, edema, hemorrhage, and acute inflammation were observed in some groups. This study shows short-term protective efficacy of erythropoietin on rat testicular injury after ischemia/reperfusion.

Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

2019 ◽  
Vol 22 (04) ◽  
pp. 122-130
Author(s):  
Rihab H Al-Mudhaffer ◽  
Laith M Abbas Al-Huseini ◽  
Saif M Hassan ◽  
Najah R Hadi
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Neurological Deficit ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

scholarly journals Circular RNA TTC3 regulates cerebral ischemia-reperfusion injury and neural stem cells by miR-372-3p/TLR4 axis in cerebral infarction

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Bo Yang ◽  
Li’e Zang ◽  
Jingwen Cui ◽  
Linlin Wei
Keyword(s):  
Stem Cells ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Neural Stem Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Cerebral Ischemia Reperfusion ◽  
The Impact

Abstract Background Stroke serves as a prevalent cerebrovascular disorder with severe cerebral ischemia/reperfusion (CIR) injury, in which neural stem cells (NSCs) play critical roles in the recovery of cerebral function. Circular RNAs (circRNAs) have been widely found to participate in stroke and NSC modulation. However, the role of circRNA TTC3 (circTTC3) in the regulation of CIR injury and NSCs remains elusive. Here, we aimed to explore the impact of circTTC3 on CIR injury and NSCs. Methods The middle cerebral artery occlusion/repression (MCAO/R) model was established in C57BL/6J mice. The primary astrocytes were isolated from the cerebellum from C57BL/6J mice. The primary NSCs were obtained from rat embryos. The effect of circTTC3 on CIR injury and NSCs was analyzed by TTC staining, qPCR, Western blot, LDH colorimetric kits, MTT assays, Annexin V-FITC Apoptosis Detection Kit, luciferase reporter gene assays, and others in the system. Results Significantly, the expression of circTTC3 was elevated in the MCAO/R mice and oxygen and glucose deprivation (OGD)-treated astrocytes. The depletion of circTTC3 attenuated cerebral infarction, neurological score, and brain water content. The OGD treatment induced apoptosis and the levels of lactate dehydrogenase (LDH) in the astrocytes, in which circTTC3 depletion reduced this phenotype in the system. Moreover, the depletion of circTTC3 promoted the proliferation and upregulated the nestin and β-tubulin III expression in NSCs. Mechanically, circTTC3 was able to sponge miR-372-3p, and miR-372-3p can target Toll-like receptor 4 (TLR4) in NSCs. The miR-372-3p inhibitor or TLR4 overexpression could reverse circTTC3 depletion-mediated astrocyte OGD injury and NSC regulation. Conclusion Thus, we conclude that circTTC3 regulates CIR injury and NSCs by the miR-372-3p/TLR4 axis in cerebral infarction. Our finding presents new insight into the mechanism by which circTTC3 modulates CIR injury and NSC dysfunction. CircTTC3, miR-372-3p, and TLR4 may serve as potential targets for the treatment of CIR injury during stroke.

scholarly journals Effects of Ischemic Post-Conditioning on the Expressions of LC3-II and Beclin-1 in the Hippocampus of Rats after Cerebral Ischemia and Reperfusion

2019 ◽  
Vol 14 (1) ◽  
pp. 179-190 ◽  
Author(s):  
Liquan Huang ◽  
Zizhuo Liu ◽  
Lingcong Wang
Keyword(s):  
Cerebral Ischemia ◽  
Hippocampal Neurons ◽  
Ischemia Reperfusion ◽  
Beclin 1 ◽  
Sprague Dawley ◽  
Akt Inhibitor ◽  
Vessel Occlusion ◽  
Cerebral Ischemia Reperfusion ◽  
Hippocampus Neuron ◽  
Related Proteins

AbstractObjectiveTo investigate the effects of postconditioning ischemia on the expressions of the hippocampus neuron autophagy-related proteins LC3-II and Beclin-1 in rats following cerebral ischemia reperfusion.MethodsA total of 128 male Sprague–Dawley rats were randomly divided into 4 groups: control, cerebral ischemia-reperfusion (IR), cerebral ischemia post-conditioning group (IP), and PI3K/Akt inhibitor (LY294002). The rat cerebral ischemia model was established by the improved Pulsinelli four vessel occlusion method. The durations across the platform and escape latent period were recorded using the water maze experiment. The changes in cell morphology and the number of surviving hippocampal neurons were detected by hematoxylin-eosin (HE) staining. The cells with Beclin-1 and LC3-II in the hippocampal region were detected by immunohistochemical staining and Western blotting.ResultsWhen compared with the IR at 48 and 72 h, the number of platform passes increased and the escape latency time was shortened. Consequently, the HE staining detected positive cells with LC3-II and Beclin-1 increased in number at each time point in immunohistochemistry and the expressions of the LC3-II and Beclin-1 proteins were improved in the IP (P < 0.05).ConclusionsCerebral ischemic post-conditioning promoted the expressions of autophagy-related proteins LC3-II and Beclin-1 while relieving the injuries caused by cerebral ischemia reperfusion.

scholarly journals Dexmedetomidine Attenuates Myocardial Ischemia-Reperfusion Injury in Diabetes Mellitus by Inhibiting Endoplasmic Reticulum Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Jinjie Li ◽  
Ying Zhao ◽  
Nan Zhou ◽  
Longyun Li ◽  
Kai Li
Keyword(s):  
Endoplasmic Reticulum ◽  
Myocardial Ischemia ◽  
Endoplasmic Reticulum Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sham Operation ◽  
Sham Operation Group ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective. With the increasing incidence of diabetes mellitus (DM) combined with myocardial ischemia, how to reduce myocardial ischemia-reperfusion injury in DM patients has become a major problem faced by clinicians. We investigated the therapeutic effects of dexmedetomidine (DEX) on myocardial ischemia-reperfusion injury in DM rats and its effect on endoplasmic reticulum stress. Methods. SD rats with SPF grade were randomly divided into 6 groups: non-DM rats were divided into the sham operation group (NDM-S group), ischemia-reperfusion group (NDM-IR group), and dexmedetomidine group (NDM-DEX group); DM rats were divided into the diabetic sham operation group (DM-S group), diabetes-reperfusion group (DM-IR group), and diabetes-dexmedetomidine (DM-DEX) group, with 10 rats in each group. Then the effects of DEX on the changes of CK-MB and cTnT levels were examined. The effects of myocardial pathological damage and myocardial infarct size were detected. The apoptosis of cardiomyocytes was detected. The apoptosis of heart tissue cells was also tested through the expressions of cleaved caspase-3, Bcl-2, and Bax proteins. The expression of endoplasmic reticulum stress-related proteins GRP78, CHOP, ERO1α, ERO1β, and PDI was examined. The hypoxia/reoxygenation (H/R) injury cell model was established, the effects of DEX, DEX+ ERS agonist on cell apoptosis was also detected. Results. The myocardial damage of DM-IR was more severe than that of NDM-IR rats. DEX could reduce the expression of CK-MB and cTnT, reduce pathological damage, and reduce scar formation and improve fibrosis. DEX can reduce the expression of GRP78, CHOP, ERO1α, ERO1β, and PDI proteins in vivo and in vitro. And the effect of DEX on cell apoptosis could be blocked by ERS agonist. Conclusion. DEX attenuates myocardial ischemia-reperfusion injury in DM rats and H/R injury cell, which is associated with the reduction of ERS-induced cardiomyocyte apoptosis.

scholarly journals Electroacupuncture Alleviates Cerebral Ischemia/Reperfusion Injury in Rats by Histone H4 Lysine 16 Acetylation-Mediated Autophagy

2020 ◽  
Vol 11 ◽  
Author(s):  
Shu-Ying Xu ◽  
He-Qun Lv ◽  
Wen-Qian Li ◽  
Hao Hong ◽  
Yong-Jun Peng ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Histone H4 ◽  
Sprague Dawley ◽  
Cerebral Ischemia Reperfusion ◽  
Histone H4 Acetylation ◽  
Sirt1 Inhibitor ◽  
Sirna Group

Background: Electroacupuncture (EA) treatment in ischemic stroke has been highlighted recently; however, the specific mechanism is still elusive. Autophagy is considered a new target for cerebral ischemia/reperfusion (I/R), but whether it plays a role of protecting or causing rapid cell apoptosis remains unclear. Studies have reported that the reduction in lysine 16 of histone H4 acetylation coheres with autophagy induction. The primary purpose of the study was to explore whether EA could alleviate I/R via autophagy-mediated histone H4 lysine 16 acetylation in the middle cerebral artery occlusion (MCAO) rat model.Methods: One hundred and twenty male Sprague-Dawley rats were divided into five groups: control group, MCAO group, MCAO+EA group, MCAO+EA+hMOF siRNA group, and MCAO+EA+Sirt1 inhibitor group. EA was applied to “Baihui” (Du20) and “Renzhong” (Du26) at 5 min after modeling and 16 h after the first EA intervention. The structure and molecular markers of the rat brain were evaluated.Results: EA significantly alleviated I/R injury by upregulating the expressions of Sirt1, Beclin1, and LC3-II and downregulating the expressions of hMOF and H4K16ac. In contrast, the Sirt1 inhibitor lowered the increase in Sirt1, Beclin1, and LC3-II and enhanced the level of hMOF and H4K16ac expressions associated with EA treatment. Besides, ChIP assay revealed that the binding of H4K16ac in the Beclin1 promoter region of the autophagy target gene was significantly raised in the MCAO+EA group and MCAO+EA+hMOF siRNA group.Conclusions: EA treatment inhibited the H4K16ac process, facilitated autophagy, and alleviated I/R injury. These findings suggested that regulating histone H4 lysine 16 acetylation-mediated autophagy may be a key mechanism of EA at Du20 and Du26 to treat I/R.

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