The edaravone and 3-n-butylphthalide ring-opening derivative 10b effectively attenuates cerebral ischemia injury in rats

Hua, Kai; Sheng, Xiao; Li, Tingting; Wang, Linna; Zhang, Yihua; Huang, Zhangjian; Ji, Hui

doi:10.1038/aps.2015.31

Cited by 49 publications

(31 citation statements)

References 45 publications

(42 reference statements)

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“…3 Several researchers have reported that anti-apoptosis and anti-inammation action can ameliorate the progress of I/R. 4 High mobility group box-1 (HMGB1) is generally known as a non-histone DNA binding protein, which is involved in the stabilization of DNA and the promotion of transcription. Recently, HMGB1 has been found to be passively released by necrotic cardiomyocytes in response to ischemia and it also acts as an early mediator of inammation following I/R injury.…”

Section: Introductionmentioning

confidence: 99%

Retracted Article: Chrysin attenuates myocardial ischemia–reperfusion injury by inhibiting myocardial inflammation

Nan

Yang

et al. 2018

RSC Adv.

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The aim of this study was to investigate the effects of chrysin (CH) on myocardial ischemia-reperfusion injury. Cytokines were reduced by CH in coronary artery occlusion-induced rats and also in H9C2 cells.The ST segment was also restored by CH. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that CH could alleviate myocardial injury. Results in H9C2 cells showed that CH improved heart injury in hypoxia/reoxygenation (H/R) of H9C2 cells. In addition, the expressions of the HMGB1-related inflammation pathway in rats and H9C2 cells were significantly decreased by CH. The present study shows the protective effects of CH on myocardial injury via inflammation.

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Section: Introductionmentioning

confidence: 99%

Retracted Article: Chrysin attenuates myocardial ischemia–reperfusion injury by inhibiting myocardial inflammation

Nan

Yang

et al. 2018

RSC Adv.

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“…In a murine model of cerebral ischaemia-reperfusion, NBP decreased the intracerebral levels of TNF-α and intracellular adhesion molecule-1, thereby reducing damage to brain tissue (17). In a rotenone-induced PD mouse model, NBP decreased damage to dopaminergic neurons in the midbrain (18). In accordance with these findings, the results indicated that 30 days of treatment with NBP during the establishment of an LPS-induced model significantly attenuated LPS-induced mesencephalic microglial activation in the early stages, and decreased the loss of dopaminergic neurons in addition to α-synuclein deposition in the substantia nigra in the late stages.…”

Section: Discussionsupporting

confidence: 80%

“…In the present study, it was observed that NBP inhibited the activation of microglia and decreased α-synuclein deposition and the loss of dopaminergic neurons in the substantia nigra of LPS-induced PD mice. NBP, also termed butylphthalide (C 12 H 14 O 2 ; molecular mass, 190) is an active ingredient isolated from the oil of celery seeds with multiple pharmacological effects (16)(17)(18), though the mechanisms underlying these effects remain unknown. NBP is a national class I chemical drug with independent intellectual property rights in China.…”

Section: Discussionmentioning

confidence: 99%

DL‑3‑n‑butylphthalide reduces microglial activation in lipopolysaccharide‑induced Parkinson's disease model mice

Chen

Jiang

et al. 2017

Mol Med Report

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As microglial activation is a key factor in the pathogenesis of Parkinson's disease (PD), drugs that target this process may help to prevent or delay the development of PD. The present study investigated the effects of dl‑3‑n‑butylphthalide (NBP) on microglia in a lipopolysaccharide (LPS)-induced PD mouse model. The mice were randomly divided into a blank control group, LPS control group and NBP + LPS treatment group. Mice in the treatment group were given an intragastric infusion of 120 mg/kg NBP daily for 30 days during the establishment of the PD mouse model. At 4 and 28 weeks post‑treatment, the motor behaviours of the mice in each group were observed using the rotarod test and the open field test. In addition, immunohistochemical staining was performed to determine the levels of activated microglia, tumour necrosis factor‑α and α‑synuclein, and the number of tyrosine hydroxylase (TH)‑positive cells in the substantia nigra. NBP significantly improved dyskinesia, reduced microglial activation, decreased nuclear α‑synuclein deposition and increased the survival of TH‑positive cells in the substantia nigra of LPS‑induced PD model mice. These findings suggested that NBP may exert its therapeutic effect by reducing microglial activation in a mouse model of PD.

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“…The homogenate was then centrifuged at 4000 rpm/min for 10 min at 4 °C. SOD activity and levels of MDA and GSH were measured as described previously [ 34 , 35 ]. Data were calculated in reference to the protein concentration in each sample.…”

Section: Methodsmentioning

confidence: 99%

Dimethyl Fumarate and Monomethyl Fumarate Promote Post-Ischemic Recovery in Mice

Yao

Miao

Liu

et al. 2016

Transl. Stroke Res.

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Oxidative stress plays an important role in cerebral ischemia–reperfusion injury. Dimethyl fumarate (DMF) and its primary metabolite monomethyl fumarate (MMF) are antioxidant agents that can activate the nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway and induce the expression of antioxidant proteins. Here, we evaluated the impact of DMF and MMF on ischemia-induced brain injury and whether the Nrf2 pathway mediates the effects provided by DMF and MMF in cerebral ischemia–reperfusion injury. Using a mouse model of transient focal brain ischemia, we show that DMF and MMF significantly reduce neurological deficits, infarct volume, brain edema, and cell death. Further, DMF and MMF suppress glial activation following brain ischemia. Importantly, the protection of DMF and MMF was mostly evident during the subacute stage and was abolished in Nrf2−/− mice, indicating that the Nrf2 pathway is required for the beneficial effects of DMF and MMF. Together, our data indicate that DMF and MMF have therapeutic potential in cerebral ischemia–reperfusion injury and their protective role is likely mediated by the Nrf2 pathway.Electronic supplementary materialThe online version of this article (doi:10.1007/s12975-016-0496-0) contains supplementary material, which is available to authorized users.

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The edaravone and 3-n-butylphthalide ring-opening derivative 10b effectively attenuates cerebral ischemia injury in rats

Abstract: Oral administration of compound 10b effectively attenuates rat cerebral ischemia injury.

Cited by 49 publications

References 45 publications

Retracted Article: Chrysin attenuates myocardial ischemia–reperfusion injury by inhibiting myocardial inflammation

Retracted Article: Chrysin attenuates myocardial ischemia–reperfusion injury by inhibiting myocardial inflammation

DL‑3‑n‑butylphthalide reduces microglial activation in lipopolysaccharide‑induced Parkinson's disease model mice

Dimethyl Fumarate and Monomethyl Fumarate Promote Post-Ischemic Recovery in Mice

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