&lt;p&gt;Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury&lt;/p&gt;

Han, Ming; Hu, Lin; Chen, Yang

doi:10.2147/dddt.s216156

Cited by 40 publications

(35 citation statements)

References 37 publications

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“…These enzymes can resist oxidative stress and damage produced by various internal and external stimuli, and promote the return to equilibrium of oxygen free radicals. Certain drugs and naturally extracted compounds (sulforaphane, ginkgo extract, white squash, andrographolide derivative CX-10, rutaecarpine, ginsenoside Rg1, and levocarnitine, among others) are able to protect the body from stroke damage by activating the Nrf2 signaling pathway (Alfieri et al, 2013;Chu et al, 2019;Han et al, 2019;Liu and Zhang, 2019;Yang et al, 2019). In vitro, activated Nrf2 has strong neuroprotective properties and can inhibit stroke injury mechanisms such as glutamate toxicity, H 2 O 2 exposure, and Ca 2+ overloading (Xu P. et al, 2018).…”

Section: Anti-oxidative Stress Signal Pathway Nrf2/are Signaling Pathwaymentioning

confidence: 99%

“…In theory, blocking pathways or targeting the key molecules of ROS generation can reduce the oxidative damage caused by CIRI. Some progress has been made in antioxidant treatments for CIRI (Kim et al, 2009;Hu et al, 2013;Watanabe et al, 2016;Mahmood et al, 2017;Lou et al, 2018;Song et al, 2018;Xing et al, 2018;Zhu et al, 2018;Chu et al, 2019;Han et al, 2019;Li S. et al, 2019;Liu and Zhang, 2019).…”

Section: Antioxidant Therapy In Cirimentioning

confidence: 99%

“…There are also many anti-oxidant ingredients naturallyoccurring in plants. Arabian-type polysaccharide (GBW) extracted from Ginkgo biloba, polyphenols from a variety of foods, and Sophora alopecuroides extract oxidized alkaloids all have antioxidant effects on cerebral ischemia in animals (Alfieri et al, 2013;Yang et al, 2013Yang et al, , 2019Chu et al, 2019;Han et al, 2019). In a mouse model of CIRI, it was demonstrated that a purpura extract can significantly reduce infarct size, restore the activities of antioxidants such as SOD and GSH, and decrease pro-oxidase enzyme activity by xanthine oxidase (Bora and Sharma, 2011).…”

Section: Natural Antioxidantsmentioning

confidence: 99%

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Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

299

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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Section: Anti-oxidative Stress Signal Pathway Nrf2/are Signaling Pathwaymentioning

confidence: 99%

Section: Antioxidant Therapy In Cirimentioning

confidence: 99%

Section: Natural Antioxidantsmentioning

confidence: 99%

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Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

299

197

View full text Add to dashboard Cite

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“…On one hand, NRF2-dependent antioxidant and detoxification enzymes promote the detoxification and elimination of ROS to attenuate arsenic carcinogenesis. On the other hand, NRF2 activation may provide cell proliferation or survival advantage by mediating metabolic reprogramming [56,97] and contributing to apoptotic resistance [98][99][100][101], which are important events in the process of arsenic-induced malignant transformation. Long-term exposure to an environmentally relevant dose of arsenic may induce constitutive activation of Nrf2, leading to adaptive antioxidant response, and subsequently contributing to malignant transformation [60,74,102,103].…”

Section: Nrf2-are Pathwaymentioning

confidence: 99%

The Role of Reactive Oxygen Species in Arsenic Toxicity

et al. 2020

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Arsenic poisoning is a global health problem. Chronic exposure to arsenic has been associated with the development of a wide range of diseases and health problems in humans. Arsenic exposure induces the generation of intracellular reactive oxygen species (ROS), which mediate multiple changes to cell behavior by altering signaling pathways and epigenetic modifications, or cause direct oxidative damage to molecules. Antioxidants with the potential to reduce ROS levels have been shown to ameliorate arsenic-induced lesions. However, emerging evidence suggests that constructive activation of antioxidative pathways and decreased ROS levels contribute to chronic arsenic toxicity in some cases. This review details the pathways involved in arsenic-induced redox imbalance, as well as current studies on prophylaxis and treatment strategies using antioxidants.

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“…Therefore, understanding the specific mechanisms underlying reperfusion injury is of clinical importance. Numerous studies have demonstrated that inflammation is an important pathological factor contributing to CIRI (4)(5)(6). It has also been reported that a particular type of proinflammatory programmed cell death, pyroptosis, also serves an important role in the pathogenesis of I/R injury (7).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑124 regulates cell pyroptosis during cerebral ischemia‑reperfusion injury by regulating STAT3

Sun

Feng

et al. 2020

Exp Ther Med

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Cerebral ischemia-reperfusion injury (CIRI) is the observed continuation and deterioration of ischemic injury, and currently, there are no effective treatment strategies for the condition. It has been reported that microRNAs (miRNAs) serve an important role in CIRI by regulating pyroptosis. The present study demonstrated that miRNA-124 regulated CIRI by regulating STAT3. To explore the relationship between miRNA-124/STAT3 and pyroptosis in CIRI, CIRI was simulated using a middle cerebral artery occlusion model. Subsequently, miRNA-124 expression levels were altered via the intracerebroventricular injection of miRNA-124 agonist or antagonist. The degree of brain tissue injury was assessed by conducting TTC staining and neurological function scoring. Relative miRNA-124 expression levels were determined via reverse transcription-quantitative PCR. A luciferase reporter gene system verified the targeted binding of miRNA-124 to STAT3. The expression levels of key proteins and proinflammatory cytokines associated with pyroptosis [caspase-1, gasdermin D, interleukin (IL)-18 and IL-1β] were detected via western blotting and immunohistochemistry. The increased expression levels of pyroptosis-associated proteins and proinflammatory cytokines in the I/R groups compared with the control group, indicated that pyroptosis intensified over time during CIRI, and miRNA-124 agonist significantly abrogated pyroptosis and improved neurological function compared with the control group. Furthermore, miRNA-124 inhibited STAT3 activation in a targeted manner, which also decreased the extent of pyroptosis. However, miRNA-124 antagonist reversed miR-124 agonist-mediated effects. Therefore, the present study indicated that miRNA-124 may provide neuroprotection against pyroptosis during CIRI, potentially via inhibition of the STAT3 signaling pathway.

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<p>Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury</p>

Cited by 40 publications

References 37 publications

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

The Role of Reactive Oxygen Species in Arsenic Toxicity

MicroRNA‑124 regulates cell pyroptosis during cerebral ischemia‑reperfusion injury by regulating STAT3

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