Introduction: Renal ischemia-reperfusion (IR) is responsible for injuries such as destruction or dysfunction of tubular epithelial cells with inflammatory reaction and oxidative stress. Several therapeutic methods have been tested to alleviate ischemia-perfusion injury, ranging from using anti-inflammatory drugs, antioxidants, and plants from traditional pharmacopeia to administering RNA interference. However, there is currently no effective therapeutic option available for the treatment of renal IR injury, other than supportive therapies such as renal replacement therapy or hydration. Objective: This present study aimed to evaluate the effect of Guiera senegalensis on renal ischemia reperfusion, a recognized plant for its antioxidant and anti-inflammatory properties. Materials and Methods: Twenty-four (24) adult male Wistar rats were divided into four following groups: SLAM (subjected to a median laparotomy with simulated ischemia);GUIERRA (animals that received 250 mg/kg of guierra senegalensis orally, once a day, for 5 days, with simulated renal ischemia);IR (animals that underwent laparotomy followed by clamping of bilateral renal pedicles for 45 min and followed by reperfusion);GUIERRA + IR (animals given GUIERRA at the dosage of 250 mg/kg per day, for 5 days and then subjected to renal ischemia-reperfusion). Data analysis was performed by ANOVA, and a significance level of p Results: Compared with the I/R group, rats in the GUIERRA + IR group showed reduced histopathological damage scores (p Conclusion: The results of this preliminary work suggest that Guiera senegalensis decreases the degree of tissue damage in renal ischemia-reperfusion cases. This plant seems to be a promising therapeutic;further studies could help to precise the targets of its compounds on ischemia-reperfusion pathways.
With the wide application of thrombolytic drugs and the advancement of endovascular therapeutic techniques, the recanalization treatment of acute artery occlusion in ischemic stroke (IS) has made a leap forward, but ischemic brain tissues still face ischemia-reperfusion injury after recanalization. Nowadays, effective neurological protective agents still cannot completely resist the multiple damages of ischemia-reperfusion injury. As an iron-dependent mode of programmed cell death, ferroptosis occupies an important position in ischemia-reperfusion injury. Selenium plays a unique protective role in ischemia-reperfusion injury as an active site element in the center of glutathione peroxidase. Therefore, the study mainly aims to review the protective role of selenium in IS and the related mechanisms, as well as the effect of selenium on the risk factors of IS.
Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Current studies have elucidated the neuroprotective role of the sirtuin protein family(Sirtuins)in modulating cerebral ischemia-reperfusion injury.However,the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration.In this review,the origin and research progress of Sirtuins are summarized,suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury,including inflammation,oxidative stress,blood-brain barrier damage,apoptosis,pyroptosis,and autophagy.The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways,such as nuclear factor-kappa B signaling,oxidative stress mediated by adenosine monophosphate-activated protein kinase,and the forkhead box O.This review also summarizes the potential of endogenous substances,such as RNA and hormones,drugs,dietary supplements,and emerging therapies that regulate Sirtuins expression.This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors.While Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury,most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans,potentially influencing the efficacy of Sirtuinstargeting drug therapies.Overall,this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.
Zi YeRunqing LiuHangxing WangAizhen ZuoCen JinNan WangHuiqi SunLuqian FengHua Yang
Increasing evidence of the significant clinical value of protection against ischemia/reperfusion injury has contributed to the realization of the independent importance of this approach in improving prognosis and reducing cardiovascular mortality.Extracellular vesicles(EVs)derived by adipose mesenchymal stem cells may mediate the paracrine effects of stem cells and provide regenerative and anti-inflammatory properties,which are enhanced byγ-aminobutyric acid.The protective effects on cardiac myocytes may result from the EV embarked by miR-21-5p,which is a target for thioredoxin-interacting protein,regulating the formation of thioredoxin-interacting protein-thioredoxin complexes and subsequently enhancing the antioxidant activity of thioredoxin.It has been found thatγ-aminobutyric acid governs myocardial bioenergetics through suppressing inflammation and supporting mitochondrial structure.Finally,stem cell-based cell-free therapy based on adipose-derived stem cell EVs is considered a promising approach to individualized management of ischemia-induced cardiomyopathy.
Post-reperfusion syndrome(PRS)in liver transplant recipients remains one of the most dreaded complications in liver transplant surgery.PRS can impact the short-term and long-term patient and graft outcomes.The definition of PRS has evolved over the years,from changes in arterial blood pressures and heart and/or de-creases in the systemic vascular resistance and cardiac output to including the fibrinolysis and grading the severity of PRS.However,all that did not reflect on the management of PRS or its impact on the outcomes.In recent years,new scientific techniques and new technology have been in the pipeline to better understand,manage and maybe prevent PRS.These new methods and techniques are still in the infancy,and they have to be proven not in prevention and management of PRS but their effects in the patient and graft outcomes.In this article,we will review the long history of PRS,its definition,etiology,mana-gement and most importantly the new advances in science and technology to prevent and properly manage PRS.
Hepatic steatosis is prevalent worldwide and is characterized as excessive lipid accumulation with/without inflammation and injury in the liver.Hepatic ischemia-reperfusion(HIR)injury commonly occurs in the process of hemorrhagic shock,liver surgery,and liver transplantation,and impairs liver function by inhibiting the electron transport chain in mitochondria during ischemia stage and producing large amount of reactive oxygen species(RoS)during reperfusion stage.
目的探讨丹参素干预心肌缺血/再灌注损伤(MIRI)大鼠的作用及其机制。方法采用左前降支动脉闭塞30 min后再灌注3 h构建MIRI大鼠模型。将60只大鼠随机分为假手术组、模型组及丹参素5、15、25 mg/kg组,每组12只。假手术组大鼠进行相同的手术操作,LAD穿线但不结扎。丹参素组在再灌注开始时ip丹参素5、15、25 mg/kg,每天1次,连续给药14 d。将另外60只大鼠随机分为假手术组、模型组、丹参素(25 mg/kg)组、erastin组和丹参素+erastin组,每组12只。丹参素组大鼠在再灌注开始时ip丹参素25 mg/kg,erastin组在MIR手术前1 h ip erastin 10μmol/L,丹参素+erastin组大鼠在再灌注开始时ip丹参素25 mg/kg,在MIR手术前1 h ip erastin 10μmol/L,每天1次,连续给药14 d。采用试剂盒检测心肌组织中氧化应激指标超氧化物歧化酶(SOD)、谷胱甘肽活性(GSH)和丙二醛(MDA)的活性,铁的含量,炎症因子白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α),肌酸激酶(CK)和乳酸脱氢酶(LDH)水平,以及α-平滑肌肌动蛋白(α-SMA)和胶原蛋白Ⅱ(CollagenⅡ)水平;通过心电图检测血流动力学参数左心室收缩压(LVSP)、左心室舒张末压(LVEDP)、左心室压力最大上升速率(+dp/dtmax)和左心室压力最大下降速率(−dp/dtmax)水平;采用苏木精–伊红(HE)染色观察心肌病理变化,TUNEL染色观察心肌细胞情况,Masson染色观察心肌纤维化程度;蛋白免疫印迹法检测心肌损伤关键蛋白酰基辅酶A合成酶长链家族成员4(ACSL4)、谷胱甘肽过氧化物酶4(GPX4)、核因子E_(2)相关因子2(Nrf2)、血红素氧合酶-1(HO-1)和核Nrf2表达水平。结果与模型组相比,丹参素组SOD及GSH活性明显升高,MDA活性和铁含量明显降低(P<0.01);IL-6、IL-1β和TNF-α水平明显降低(P<0.01);CK和LDH水平显著降低(P<0.01);α-SMA和CollagenⅡ水平显著降低(P<0.01);LVEDP水平显著降低,LVSP、+dp/dtmax和−dp/dtmax水平显著升高(
