Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia–reperfusion injury

Zhao, Nan; Gao, Yuhe; Jia, Hao; Jiang, Xicheng

doi:10.1007/s10495-023-01824-6

Cited by 14 publications

(3 citation statements)

References 291 publications

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“…Previous research has confirmed that ischemia can cause degeneration and necrosis of massive neurons along with severe neurological defects ( Zhao et al, 2023b ). Angiogenesis of ischemic brain tissue and the addition of new collateral circulation can increase blood supply to improve ischemic brain function ( Hatakeyama, Ninomiya & Kanazawa, 2020 ).…”

Section: Discussionmentioning

confidence: 93%

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Sun,

Wu,

Lan

et al. 2024

PeerJ

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Ischemic stroke (IS) is a disease with a high mortality and disability rate worldwide, and its incidence is increasing per year. Angiogenesis after IS improves blood supply to ischemic areas, accelerating neurological recovery. β-asarone has been reported to exhibit a significant protective effect against hypoxia injury. The ability of β-asarone to improve IS injury by inducing angiogenesis has not been distinctly clarified. The experimental rats were induced with middle cerebral artery occlusion (MCAO), and oxygen-glucose deprivation (OGD) model cells were constructed using human microvascular endothelial cell line (HMEC-1) cells. Cerebral infarction and pathological damage were first determined via triphenyl tetrazolium chloride (TTC) and hematoxylin and eosin (H&E) staining. Then, cell viability, apoptosis, and angiogenesis were assessed by utilizing cell counting kit-8 (CCK-8), flow cytometry, spheroid-based angiogenesis, and tube formation assays in OGD HMEC-1 cells. Besides, angiogenesis and other related proteins were identified with western blot. The study confirms that β-asarone, like nimodipine, can ameliorate cerebral infarction and pathological damage. β-asarone can also upregulate vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) and induce phosphorylation of p38. Besides, the study proves that β-asarone can protect against IS injury by increasing the expression of VEGFA. In vitro experiments affirmed that β-asarone can induce viability and suppress apoptosis in OGD-mediated HMEC-1 cells and promote angiogenesis of OGD HMEC-1 cells by upregulating VEGFA. This establishes the potential for β-asarone to be a latent drug for IS therapy.

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Section: Discussionmentioning

confidence: 93%

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Sun,

Wu,

Lan

et al. 2024

PeerJ

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“…Ischemic stroke could cause devastating brain damage and functional deficits, but the detail molecular mechanism is still unclear. Ample evidence suggests that programmed cell death pathways and inflammatory response might be critical [2,20], such as apoptosis [21], necrosis [22], autophagy [23], ferroptosis [24], and pyroptosis [25]. Previous studies show that these pathways have respective manners in the distinct regions after ischemia/reperfusion attack.…”

Section: Discussionmentioning

confidence: 99%

Caspase-1 deletion reveals pyroptosis participates in neural damage induced by cerebral ischemia/reperfusion in tMCAO model mice

Hao,

Xue,

Zhou

et al. 2024

NeuroReport

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Pyroptosis, a form of programmed cell death, drives inflammation in the context of cerebral ischemia/reperfusion. The molecular mechanism of pyroptosis underlying ischemia/reperfusion, however, is not fully understood. The transient middle cerebral artery occlusion was applied to wild-type and caspase-1 knockout mice. 2,3,5-Triphenyltetrazolium chloride-staining and immunohistochemistry were used to identify the ischemic region, and western blot and immunofluorescence for the examination of neuronal pyroptosis. The expression of inflammatory factors and the behavioral function assessments were further conducted to examine the effects of caspase-1 knockout on protection against ischemia/reperfusion injury. Ischemia/reperfusion injury increased pyroptosis-related signals represented by the overexpression of pyroptosis-related proteins including caspase-1 and gasdermin D (GSDMD). Meanwhile, the number of GSDMD positive neurons increased in penumbra by immunofluorescence staining. Compared with wild-type mice, those with caspase-1 knockout exhibited decreased levels of pyroptosis-related proteins following ischemia/reperfusion. Furthermore, ischemia/reperfusion attack-induced brain infarction, cerebral edema, inflammatory factors, and neurological outcomes were partially improved in caspase-1 knockout mice. The data indicate that pyroptosis participates in ischemia/reperfusion induced-damage, and the caspase-1 might be involved, it provides some new insights into the molecular mechanism of ischemia.

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“…For instance, selenium can inhibit autophagy by modulating the PI3K/AKT/mTOR signaling pathway, effectively preventing BBB injury following CIRI, particularly under hyperglycemic conditions. [55] Curcumin, [56] Cornin, [57] and Cyclo-(Phe-Tyr) [58] also inhibit excessive autophagy through this pathway to offer neuroprotection and maintain BBB integrity. Additionally, (-)-Epigallocatechin-3-gallate (EGCG), a bioactive component found in green tea, can inhibit autophagy via the AKT/AMPK/mTOR phosphorylation pathway, thus preventing further reperfusion injury in the mouse brain.…”

Section: Discussionmentioning

confidence: 99%

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

Shi,

Xu,

et al. 2023

Medicine

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Background: Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process that typically occurs during the treatment of ischemia, with limited therapeutic options. Autophagy plays a vital role during the reperfusion phase and is a potential therapeutic target for preventing and treating cerebral ischemia-reperfusion injury. Methods: We conducted a comprehensive search of the Web of Science Core Collection for publications related to cerebral ischemia-reperfusion injury with autophagy, published between January 1, 2008, and January 1, 2023. We analyzed the selected publications using VOSviewer, CiteSpace, and other bibliometric tools. Results: Our search yielded 877 relevant publications. The field of autophagy in cerebral ischemia-reperfusion injury has grown rapidly since 2016. China has been the leading contributor to publications, followed by the USA and Iran. Chen Zhong and Qin Zhenghong have been influential in this field but have yet to reach all groups. In addition, there has been a shortage of collaboration among authors from different institutions. Our literature and keyword analysis identified Neurovascular protection (#11 Neuroprotective, #13 Neurovascular units, etc) and Inflammation (NLRP3 inflammasome) as popular research directions. Furthermore, the terms “Blood-Brain Barrier,” “Mitophagy,” and “Endoplasmic reticulum stress” have been frequently used and may be hot research topics in the future. Conclusions: The role of autophagy in cerebral ischemia-reperfusion injury remains unclear, and the specific mechanisms of drugs used to treat ischemia-reperfusion injury still need to be explored. This work outlines the changing trends in investigating cerebral ischemia-reperfusion injury involving autophagy and suggests future lines of inquiry.

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Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia–reperfusion injury

Cited by 14 publications

References 291 publications

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Caspase-1 deletion reveals pyroptosis participates in neural damage induced by cerebral ischemia/reperfusion in tMCAO model mice

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

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