Beneficial consequences of Lupeol on middle cerebral artery-induced cerebral ischemia in the rat involves Nrf2 and P38 MAPK modulation

Zhang, Zhiyuan; Xu, Chongfu; Hao, Jiheng; Zhang, Meng; Wang, Zidong; Yin, Tengkun; Lin, Kai; Liu, Weidong; Jiang, Qunlong; Li, Zhongchen; Wang, Dan; Mao, Zhiqi; Tong, Huaiyu; Zhang, Liyong

doi:10.1007/s11011-020-00565-8

Cited by 14 publications

(10 citation statements)

References 35 publications

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“…Thus, necroptosis is also considered a proinflammatory cell death mode, and blocking necroptosis can decrease inflammation [ 45 ]. Furthermore, study has shown that proinflammatory mediators, such as TNF-α, IL-1β, and IL-6, and anti-inflammatory mediators, such as IL-10, are involved in the inflammatory responses induced by CIR [ 46 ]. In the present study, we tested the levels of proinflammatory (TNF-α, IL-1β, and IL-6) and anti-inflammatory (IL-10) cytokines in the serum and peri-infarct tissues to determine whether CHIP exerts anti-inflammatory effects in MCAO mouse models.…”

Section: Discussionmentioning

confidence: 99%

CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation

Yao

Zhang

et al. 2021

Aging

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Blood reperfusion of ischemic cerebral tissue may cause cerebral ischemia-reperfusion (CIR) injury. Necroptosis and inflammation have been demonstrated to be involved in the disease-related process of CIR injury. The E3 ubiquitin ligase carboxyl terminus of Hsp70-interacting protein (CHIP) can modulate multiple cellular signaling processes, including necroptosis and inflammation. Numerous studies have demonstrated the neuroprotective effects of CHIP on multiple central nervous system (CNS) diseases. However, the effects of CHIP on CIR injury have not been fully explored. We hypothesize that CHIP can exert neuroprotective effects by attenuating necroptosis and inflammation during CIR injury. In the present study, adult wild-type (WT) C57BL/6 mice and CHIP knock-in (KI) mice with a C57BL/6 background and CHIP overexpression in neural tissue underwent middle cerebral artery occlusion (MCAO) surgery to simulate CIR onset. Our data indicated that CHIP expression in the peri-infarct tissue was markedly increased after MCAO surgery. Compared with WT mice, CHIP KI mice significantly improved neurological deficit scores, decreased cerebral infarct volume, and attenuated brain edema and neuronal damage. Meanwhile, CHIP overexpression attenuated necroptosis and inflammation induced by MCAO surgery. These findings indicated that overexpression of CHIP might exert neuroprotective effects by attenuating necroptosis and inflammation during CIR injury, and increasing CHIP levels may be a potential strategy in cerebrovascular disease therapy.

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Section: Discussionmentioning

confidence: 99%

CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation

Yao

Zhang

et al. 2021

Aging

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“…Medicarpin has hydroxyl radical scavenging activity [56]. Isoliquiritigenin, ursolic acid, and lupeol alleviate the neuronal damage induced by ischemia [57][58][59]. Liquid chromatography-mass spectrometry studies need to be conducted to determine the functional components of CVE to show neuroprotective actions and mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Cissus verticillata Extract Decreases Neuronal Damage Induced by Oxidative Stress in HT22 Cells and Ischemia in Gerbils by Reducing the Inflammation and Phosphorylation of MAPKs

Kim

Kwon

Jung

et al. 2021

Plants

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In the present study, we examined the effects of Cissus verticillata leaf extracts (CVE) against hydrogen peroxide (H2O2)- and ischemia-induced neuronal damage in HT22 cells and gerbil hippocampus. Incubation with CVE produced concentration-dependent toxicity in HT22 cells. Significant cellular toxicity was observed with >75 μg/mL CVE. CVE treatment at 50 μg/mL ameliorated H2O2-induced reactive oxygen species formation, DNA fragmentation, and cell death in HT22 cells. In addition, incubation with CVE significantly mitigated the increase in Bax and decrease in Bcl-2 induced by H2O2 treatment in HT22 cells. In an in vivo study, the administration of CVE to gerbils significantly decreased ischemia-induced motor activity 1 d after ischemia, as well as neuronal death and microglial activation 4 d after ischemia, respectively. CVE treatment reduced the release of interleukin-1β, interleukin-6, and tumor necrosis factor-α 6 h after ischemia. Furthermore, CVE treatment significantly ameliorated ischemia-induced phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2, and p38. These results suggest that CVE has the potential to reduce the neuronal damage induced by oxidative and ischemic stress by reducing the inflammatory responses and phosphorylation of MAPKs, suggesting that CVE could be a functional food to prevent neuronal damage induced by ischemia.

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“…There was a evidence that lupeol, one component of AT, decreased lipid peroxidation level in the early stage of hypercholesterolemia artery atherosclerosis [ 40 ]. It was demonstrated that lupeol could exert a protective effect against cerebral I/R by activating Nrf2 and inhibiting p38-MAPK, with decreasing proinflammatory factors TNF- α , IL-1 β , and IL-6, increasing anti-inflammatory factor IL-10, and suppressing oxidative stress level [ 41 ]. JNK and p38 MAPK promotes the expression of JUN to promote the proatherosclerosis process.…”

Section: Discussionmentioning

confidence: 99%

Revealing the Pharmacological Mechanism of Acorus tatarinowii in the Treatment of Ischemic Stroke Based on Network Pharmacology

Liu

Zhao

Liu

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Aim. Stroke is the second significant cause for death, with ischemic stroke (IS) being the main type threatening human being’s health. Acorus tatarinowii (AT) is widely used in the treatment of Alzheimer disease, epilepsy, depression, and stroke, which leads to disorders of consciousness disease. However, the systemic mechanism of AT treating IS is unexplicit. This article is supposed to explain why AT has an effect on the treatment of IS in a comprehensive and systematic way by network pharmacology. Methods and Materials. ADME (absorbed, distributed, metabolized, and excreted) is an important property for screening-related compounds in AT, which were screening out of TCMSP, TCMID, Chemistry Database, and literature from CNKI. Then, these targets related to screened compounds were predicted via Swiss Targets, when AT-related targets database was established. The gene targets related to IS were collected from DisGeNET and GeneCards. IS-AT is a common protein interactive network established by STRING Database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were analysed by IS-AT common target genes. Cytoscape software was used to establish a visualized network for active compounds-core targets and core target proteins-proteins interactive network. Furthermore, we drew a signal pathway picture about its effect to reveal the basic mechanism of AT against IS systematically. Results. There were 53 active compounds screened from AT, inferring the main therapeutic substances as follows: bisasaricin, 3-cyclohexene-1-methanol-α,α,4-trimethyl,acetate, cis,cis,cis-7,10,13-hexadecatrienal, hydroxyacoronene, nerolidol, galgravin, veraguensin, 2′-o-methyl isoliquiritigenin, gamma-asarone, and alpha-asarone. We obtained 398 related targets, 63 of which were the same as the IS-related genes from targets prediction. Except for GRM2, remaining 62 target genes have an interactive relation, respectively. The top 10 degree core target genes were IL6, TNF, IL1B, TLR4, NOS3, MAPK1, PTGS2, VEGFA, JUN, and MMP9. There were more than 20 terms of biological process, 7 terms of cellular components, and 14 terms of molecular function through GO enrichment analysis and 13 terms of signal pathway from KEGG enrichment analysis based on P < 0.05 . Conclusion. AT had a therapeutic effect for ischemic via multicomponent, multitarget, and multisignal pathway, which provided a novel research aspect for AT against IS.

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Beneficial consequences of Lupeol on middle cerebral artery-induced cerebral ischemia in the rat involves Nrf2 and P38 MAPK modulation

Cited by 14 publications

References 35 publications

CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation

CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation

Cissus verticillata Extract Decreases Neuronal Damage Induced by Oxidative Stress in HT22 Cells and Ischemia in Gerbils by Reducing the Inflammation and Phosphorylation of MAPKs

Revealing the Pharmacological Mechanism of Acorus tatarinowii in the Treatment of Ischemic Stroke Based on Network Pharmacology

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