Preserving mitochondrial function by inhibiting GRP75 ameliorates neuron injury under ischemic stroke

Wen, Bin; Xu, Kai; Huang, Rui; Jiang, Teng; Wang, Jian; Chen, Jiehui; Chen, Juan; He, Benhong

doi:10.3892/mmr.2022.12681

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…1 ) ( 28 ). While Inhibition of the heat shock 75-kDa glucose-regulated protein was able to effectively ameliorate mitochondrial calcium overload and alleviate the ischemic stroke ( 39 ).…”

Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1β release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.

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“…1 ) ( 28 ). While Inhibition of the heat shock 75-kDa glucose-regulated protein was able to effectively ameliorate mitochondrial calcium overload and alleviate the ischemic stroke ( 39 ).…”

Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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“…Mitochondrial dysfunction is an established member of IS pathophysiology. Indeed, the mitochondrial response, including calcium overload, disrupted mitochondrial quality control and dynamics, and excessive production of reactive oxygen species, is an integral contributor to post-IS neuronal loss [62,63,65]. These mechanistic changes are initiated by severe oxygen and glucose deprivation secondary to reduction of regional cerebral blood flow, which effectively depletes adenosine triphosphate reserves [62].…”

Section: Ischemic Strokementioning

confidence: 99%

“…For instance, mitochondrial fission is mediated by cytosolic protein Drp1 and, secondarily, outer mitochondrial membrane fusion protein Mfn1/2 [62]. Absence of the latter has interestingly been linked to mitochondrial fragmentation [58,65]. Moreover, expression of inner mitochondrial membrane fusion protein Opa1 evidence progressive downregulation in animal models of middle cerebral artery occlusion [62].…”

Section: Ischemic Strokementioning

confidence: 99%

Mechanisms of Mitochondrial Oxidative Stress in Brain Injury: From Pathophysiology to Therapeutics

Nguyen

Patel

Kioutchoukova

et al. 2023

Oxygen

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Mitochondrial oxidative stress has been implicated in various forms of brain injury, both traumatic and non-traumatic. Due to its oxidative demand, the brain is intimately dependent on its mitochondrial functioning. However, there remains appreciable heterogeneity in the development of these injuries regarding ROS and their effect on the sequelae. These include traumatic insults such as TBIs and intracranial hemorrhaging secondary to this. In a different vein, such injuries may be attributed to other etiologies such as infection, neoplasm, or spontaneous hemorrhage (strokes, aneurysms). Clinically, the manner of treatment may also be adjusted in relation to each injury and its unique progression in the context of ROS. In the current review, then, the authors highlight the role of mitochondrial ROS in various forms of brain injury, emphasizing both the collective and unique elements of each form. Lastly, these narratives are met with the current therapeutic landscape and the role of emerging therapies in treating reactive oxygen species in brain injuries.

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“…Different mechanisms involved in the pathological process of ischemic stroke include neuron apoptosis, necrosis, and ferroptosis. [46] Despite the extensive research for prevention of neuronal loss, no neuroprotective agents are widely available for clinical applications. [47] Brief transient ischemia induces selective neuronal loss in the hippocampus.…”

Section: Effect Of P Reptans Root Extract On Inhibitory Passive Avoid...mentioning

confidence: 99%

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Noorgaldi,

Sarkala,

Enayati

et al. 2023

Archiv der Pharmazie

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Stroke is the most common cause of death among neurological diseases. The protective effects of Potentilla reptans L. include antioxidative, anti‐inflammatory, and antiapoptotic effects. In this study, the brain protection and beta‐amyloid effects of P. reptans root extract were investigated in the rat brain ischemia/reperfusion (IR) model. Forty male Wistar rats were randomly divided into five groups (n = 8), including IR, sham, and three groups receiving P. reptans with concentrations of 0.025, 0.05, and 0.1 (g/kg/b.w.), which were injected daily for 7 days. For the IR model, the common carotid artery was occluded bilaterally for 8 min. All injections were intraperitoneal (IP). The shuttle box test was used to measure passive avoidance memory. Then the brain tissue was extracted for the histological examination of neuron counts and β‐amyloid plaques using a morphometric technique, and finally, Statistical Package for the Social Sciences software was used for statistical analysis of the data. Pretreatment with P. reptans improved memory impairment. Also, by examining the tissues of the CA1, CA3, and dentate gyrus areas of the hippocampus, it was observed that the number of plaques in the groups receiving P. reptans extract was reduced compared to the IR group, especially at the concentration of 0.05 g/kg/b.w. Also, P. reptans improved the number of neurons at all concentrations, in which the concentration of 0.05 g/kg/b.w. showed more effective therapeutic results. Taken together, we found that P. reptans root extract has beneficial effects on memory impairment, neuronal loss, and β‐amyloid accumulation.

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Preserving mitochondrial function by inhibiting GRP75 ameliorates neuron injury under ischemic stroke

Cited by 13 publications

References 36 publications

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Mechanisms of Mitochondrial Oxidative Stress in Brain Injury: From Pathophysiology to Therapeutics

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

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