Sinomenine Provides Neuroprotection in Model of Traumatic Brain Injury via the Nrf2–ARE Pathway

Yang, Youqing; Wang, Handong; Liu, Liwen; Li, Xiang; Wang, Qiang; Ding, Hui; Wang, Xiaoliang; Ye, Zhen-Nan; Wu, Lingyun; Zhang, Xiangsheng; Zhou, Meifang; Pān, Hào

doi:10.3389/fnins.2016.00580

Cited by 38 publications

(17 citation statements)

References 41 publications

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“…Recent studies indicated that SIN has anti-cancer effects on several cancers, such as breast cancer, hepatocellular carcinoma, and lung cancer [ 12 , 13 , 17 ]. Evidence also confirmed the neuroprotective effects of SIN [ 11 , 18 , 19 ]. Furthermore, a growing number of studies have revealed that SIN has multiple pharmacological activities, including antiangiogenic, antirheumatic, immunosuppressive effects, and anti-inflammatory effects [ 11 ].…”

Section: Discussionmentioning

confidence: 71%

Protective Effects of Sinomenine on CFA-Induced Inflammatory Pain in Rats

Yuan

Zhang

et al. 2018

Med Sci Monit

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BackgroundThe purpose of this study was to investigate the effects of sinomenine (SIN) on CFA-induced inflammatory pain in rats, and to explore the underlying molecular mechanisms.Material/MethodsTo determine the potential influences of SIN in the pathogenesis of inflammatory pain, an inflammatory pain (IP) mouse model was established and rats were treated with SIN (30 mg/kg). Behavioral tests were used to assess the MWT and TWL of the rats. ELISA assay was used to detect the level of inflammation cytokines. Western blotting and qRT-PCR were carried out to measure the related protein and mRNA expression level, respectively.ResultsWe found that the MWT and TWL of the CFA-treated rats were markedly lower than that of the control rats, and they were significantly increased by SIN administration. The results suggest that IP rats had higher levels of TNF-α, IL-1β and IL-6 compared with the control rats. SIN administration decreased the levels of TNF-α, IL-1β, and IL-6. In addition, we found that p-p65 and p-p38 expression notably decreased after SIN treatment in IP rats. Moreover, the results showed that SIN inhibited Cox-2 and PGE2 expression in IP rats.ConclusionsThe data indicate that SIN had a protective role in inflammatory pain through repressing inflammatory mediators via preventing the p38MAPK-NF-κB pathway.

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Section: Discussionmentioning

confidence: 71%

Protective Effects of Sinomenine on CFA-Induced Inflammatory Pain in Rats

Yuan

Zhang

et al. 2018

Med Sci Monit

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“…In oxidative stress, production of free radicals enhanced that result in oxidation and nitration of proteins, lipid peroxidation and DNA damage [5]. In TBI, the level of MDA is reported to be enhanced and activity of GPx and SOD reduced in the neuronal tissues [17]. Data of the study reveal that treatment with vorinostat reduces the altered parameters of oxidative stress.…”

Section: Discussionmentioning

confidence: 98%

Vorinostat: a histone deacetylases (HDAC) inhibitor ameliorates traumatic brain injury by inducing iNOS/Nrf2/ARE pathway

Xu¹,

Shi²,

Zhang³

et al. 2018

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The present investigation evaluates the protective effect of vorinostat on neuronal cells in the traumatic brain injury (TBI) and also postulates the possible mechanism of its action. Marmarou's weight-drop model was used to induce the TBI. Further, animals were treated with vorinostat 100 mg/kg intraperitoneally 30 min before the TBI induction. Neurological score and brain water content were determined in all the groups and thereafter oxidative stress parameters and adenosine triphosphate (ATP) content were determined in the neuronal tissues of TBI mice. Western blot assay and reverse transcription polymerase chain reaction (RT-PCR) was performed for the determination of the expression of several proteins in the neuronal tissues. Moreover, immunohistochemical staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was also done on the neuronal tissues of TBI mice. Data of the study reveal that treatment with vorinostat significantly reduces the altered level of grip test scores and water content in the brain of traumatic injured mice. Moreover, the altered level of oxidative stress parameters, translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and ATP content was attenuated by treating TBI mice with vorinostat. Also treatment with vorinostat ameliorates the altered expression of p-Akt, NF-κB, iNOS and caspase by the western blot assay in the neuronal tissue of TBI mice and mRNA level of HO-1 and NQO-1 significantly enhanced in vorinostat compared to the negative control group. Furthermore, the TUNEL assay also reveals that the apoptosis of neuronal cells was significantly (p < 0.01) reduced in the vorinostat-treated group compared to the negative control group. The present study concludes that vorinostat protects the neuronal injury in TBI mice by reducing the altered level of oxidative stress and inflammatory response.

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“… 7 , 8 SIN exerts neuroprotective effects in different central nervous system (CNS) diseases, including cerebral ischemia, intracerebral hemorrhage, and neurodegenerative diseases. 9 , 10 However, the mechanisms of these effects are still not well understood. Besides, few studies have addressed the neuroprotective effect of SIN in TBI.…”

Section: Introductionmentioning

confidence: 99%

Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial pathway

Wang

Zhai

et al. 2018

DDDT

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Background Sinomenine (SIN) has been shown to have protective effects against brain damage following traumatic brain injury (TBI). However, the mechanisms and its role in these effects remain unclear. This study was conducted to investigate the potential mechanisms of the protective effects of SIN. Methods The weight-drop model of TBI in Institute of Cancer Research (ICR) mice were treated with SIN or a vehicle via intraperitoneal administration 30 min after TBI. All mice were euthanized 24 h after TBI and after neurological scoring, a series of tests were performed, including brain water content and neuronal cell death in the cerebral cortex. Results The level of cytochrome c (Cyt c ), malondialdehyde (MDA), glutathione peroxidase (GPx) and superoxide dismutase 1 (SOD) were restored to some degree following the SIN treatment. The SIN treatment significantly decreased caspase-3 expression and reduced the number of positive cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and improved the survival of neuronal cells. Additionally, the pretreatment levels of MDA were restored, while Bax translocation to mitochondria and Cyt c release into the cytosol were reduced by the SIN treatment. Conclusion SIN protected neuronal cells by protecting them against apoptosis via mechanisms that involve the mitochondria following TBI.

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Sinomenine Provides Neuroprotection in Model of Traumatic Brain Injury via the Nrf2–ARE Pathway

Cited by 38 publications

References 41 publications

Protective Effects of Sinomenine on CFA-Induced Inflammatory Pain in Rats

Protective Effects of Sinomenine on CFA-Induced Inflammatory Pain in Rats

Vorinostat: a histone deacetylases (HDAC) inhibitor ameliorates traumatic brain injury by inducing iNOS/Nrf2/ARE pathway

Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial pathway

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