scholarly journals Neuroprotective effects of crocin I and II in an ischemia-reperfusion injury model

2019 ◽  
Author(s):  
Baowei Lv ◽  
Junyan Yin ◽  
Chunqing Feng ◽  
Yanhui Li
Keyword(s):  
Amino Acids ◽  
Frontal Cortex ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Synergistic Effects ◽  
Ischemia Reperfusion ◽  
Crocus Sativus ◽  
Neuroprotective Effects ◽  
Anoxic Injury ◽  
Injury Model

AbstractBackgroundCrocin I and II are derived from the medicinal plant Crocus sativus L. (Saffron), and their neuroprotective effects have been attracting more and more attention. However, their protective effect against cerebral apoplexy induced by hypoxia has not been reported. In this study, we aimed to clarify the roles of crocin I and II in protecting against ischemic injury.Materials/MethodsWe generated a rat cerebral ischemia-reperfusion injury model using a reversible cerebral artery occlusion suture method and found changes in amino acid neurotransmitters in the frontal cortex after drug administration. We also identified changes in mRNA expression of Bcl2, Bax, Casp3, P38, and NFkb1 in the frontal cortex and changes in antioxidant indices in the brain.ResultsCrocin I and II both had protective effects on ischemic/anoxic injury in vivo by downregulating the expression of Casp3 and Nfkb1 mRNA and the steady-state levels of excitatory amino acids/inhibitory amino acids during ischemia and reperfusion and by improving the total antioxidant capacity and total superoxide dismutase activities during ischemia. We also found that crocin I and II had synergistic effects when used together.ConclusionsThese findings displayed that crocin I and II could protect animal model against ischemic and anoxic injury and provided new evidence for both molecules’ potential medicinal value.

scholarly journals Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Chong Huang ◽  
Yan Chen ◽  
Bin Lai ◽  
Yan-Xia Chen ◽  
Cheng-Yun Xu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Akt Pathway ◽  
Acute Renal Injury ◽  
Injury Model ◽  
Renal Ischemia Reperfusion Injury

Abstract Background Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown. Methods An in vitro HK-2 cells with anoxia-reoxygenation injury model (In vitro simulated ischemic injury disease) and an in vivo rat renal ischemia-reperfusion injury model were used in this study. The expression levels of SP1, miR-205 and PTEN were detected by RT-qPCR, and the protein expression levels of SP1, p62, PTEN, AKT, p-AKT, LC3II, LC3I and Beclin-1 were assayed by western blot. Cell proliferation was assessed by MTT assay, and the cell apoptosis was detected by flow cytometry. The secretions of IL-6 and TNF-α were detected by ELISA. The targeted relationship between miR-205 and PTEN was confirmed by dual luciferase report assay. The expression and positioning of LC-3 were observed by immunofluorescence staining. TUNEL staining was used to detect cell apoptosis and immunohistochemical analysis was used to evaluate the expression of SP1 in renal tissue after ischemia-reperfusion injury in rats. Results The expression of PTEN was upregulated while SP1 and miR-205 were downregulated in renal ischemia-reperfusion injury. Overexpression of SP1 protected renal tubule cell against injury induced by ischemia-reperfusion via miR-205/PTEN/Akt pathway mediated autophagy. Overexpression of SP1 attenuated renal ischemia-reperfusion injury in rats. Conclusions SP1 overexpression restored autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

scholarly journals miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

2021 ◽  
Vol 12 (1) ◽  
pp. 210-217
Author(s):  
Yibiao Wang ◽  
Min Xu
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Luciferase Assay ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion

Abstract Background This study aimed to explore the role of miR-380-5p in cerebral ischemia/reperfusion (CIR) injury-induced neuronal cell death and the potential signaling pathway involved. Methodology Human neuroblastoma cell line SH-SY5Y cells were used in this study. Oxygen and glucose deprivation/reperfusion (OGD/R) model was used to mimic ischemia/reperfusion injury. CCK-8 assay and flow cytometry were used to examine cell survival. Quantitative real time PCR (RT-qPCR) assay and Western blotting were used to measure the change of RNA and protein expression, respectively. TargetScan and Luciferase assay was used to confirm the target of miR-380-5p. Malondialdehyde (MDA) superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) were measured using commercial kits. Results miR-380-5p was downregulated in SH-SY5Y cells after OGD/R. Cell viability was increased by miR-380-5p, while cell apoptosis was reduced by miR-380-5p mimics. MDA was reduced by miR-380-5p mimics, while SOD and GSHPx were increased by miR-380-5p. Results of TargetScan and luciferase assay have showed that BACH1 is the direct target of miR-380-5p. Expression of NRF2 was upregulated after OGD/R, but was not affected by miR-380-5p. mRNA expression of HO-1 and NQO1 and ARE activity were increased by miR-380-5p. Overexpression of BACH1 reversed the antioxidant and neuroprotective effects of miR-380-5p. Conclusion miR-380-5p inhibited cell death induced by CIR injury through target BACH1 which also facilitated the activation of NRF2, indicating the antioxidant and neuroprotective effects of miR-380-5p.

scholarly journals Comparison of the protective effects of desflurane and propofol anesthesia in rats: a hepatic ischemia-reperfusion injury model

2013 ◽  
Vol 43 ◽  
pp. 592-598
Author(s):  
Ayca TAŞ TUNA ◽  
Cengiz Bekir DEMİREL ◽  
Yusuf ÜNAL ◽  
Aslıhan ÇAVUNT BAYRAKTAR ◽  
Demet YILMAZER ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatic Ischemia ◽  
Injury Model ◽  
Hepatic Ischemia Reperfusion

scholarly journals Neuroprotective Effects of Mitochondria-Targeted Plastoquinone and Thymoquinone in a Rat Model of Brain Ischemia/Reperfusion Injury

Molecules ◽  
2015 ◽  
Vol 20 (8) ◽  
pp. 14487-14503 ◽  
Author(s):  
Denis Silachev ◽  
Egor Plotnikov ◽  
Ljubava Zorova ◽  
Irina Pevzner ◽  
Natalia Sumbatyan ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Brain Ischemia ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects

scholarly journals VALIDATION OF INFARCT CHARACTERIZATION IN A PORCINE ISCHEMIA REPERFUSION INJURY MODEL

2013 ◽  
Vol 61 (10) ◽  
pp. E617
Author(s):  
Kaori Nakagawa ◽  
Fumiaki Ikeno ◽  
Yuka Matsuura ◽  
Jennifer Lyons ◽  
Patricia Nguyen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Injury Model

scholarly journals Neuroprotective effects of FK-506, l-carnitine and azathioprine on spinal cord ischemia-reperfusion injury

2004 ◽  
Vol 25 (1) ◽  
pp. 105-110 ◽  
Author(s):  
Serdar Akgun ◽  
Atike Tekeli ◽  
Ozlem Kurtkaya ◽  
Ali Civelek ◽  
Selim C Isbir ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Neuroprotective Effects ◽  
Fk 506
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