Publications by authors named "Reai Shan"

2 Publications

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Neuroprotective Effects of Four Different Fluids on Cerebral Ischemia/Reperfusion Injury in Rats through Stabilization of the Blood-Brain Barrier.

Eur J Neurosci 2021 Jul 14. Epub 2021 Jul 14.

Key Laboratory of Prevention and treatment of cardiovascular and cerebrovascular diseases of Ministry of Education, Gannan Medical University, Ganzhou, China.

Protecting the blood-brain barrier (BBB) is a potential strategy to treat cerebral ischemic injury. We previously reported that hypertonic sodium chloride hydroxyethyl starch 40 (HSH) treatment alleviates brain injury induced by transient middle cerebral artery occlusion (tMCAO). However, other fluids, including 20% mannitol (MN), 3% hypertonic sodium chloride (HTS), and hydroxyethyl starch 130/0.4 solution (HES), have the same effect as HSH in cerebral ischemia/reperfusion injury (CI/RI) remains unclear. The present study evaluated the protective effects of these four fluids on the BBB in tMCAO rats. Sprague-Dawley (SD) rats were randomly assigned to 6 groups. A CI/RI rat model was established by tMCAO for 120 min followed by 24 h of reperfusion. The sham and tMCAO groups were treated with normal saline (NS), while the other four groups were treated with the four fluids. After 24 h of reperfusion, neurological function, brain edema, brain infarction volume, permeability of the BBB, cortical neuron loss, and protein and mRNA expression were assessed. The four fluids (especially HSH) alleviated neurological deficits and decreased the infarction volume, brain edema, BBB permeability and cortical neuron loss induced by tMCAO. The expression levels of GFAP, IL-1β, TNF-α, MMP-9, MMP-3, AQP4, MMP-9, PDGFR-β and RGS5 were decreased, while the expression levels of laminin and claudin-5 were increased. These data suggested that small-volume reperfusion using HSH, HES, MN and HTS ameliorated CI/RI, probably by attenuating BBB disruption and postischemic inflammation, with HSH exerting the strongest neuroprotective effect.
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http://dx.doi.org/10.1111/ejn.15385DOI Listing
July 2021

Celastrol ameliorates inflammatory pain and modulates HMGB1/NF-κB signaling pathway in dorsal root ganglion.

Neurosci Lett 2019 01 2;692:83-89. Epub 2018 Nov 2.

Department of Physiology, Gannan Medical University, Ganzhou, 341000, PR China; Institute of Pain Medicine, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, PR China. Electronic address:

Evidences reported that high mobility group box 1 (HMGB1) played a pivotal role in the modulation of chronic inflammatory pain. Celastrol, a bioactive component extracted from Tripterygium wilfordii Hook, possesses anti-inflammatory activity, but the underlying mechanism remains to be fully clarified. We aim to investigate whether HMGB1 in dorsal root ganglion (DRG) participates in the effect of celastrol on inflammatory pain. Complete Freund's adjuvant (CFA)-induced inflammatory pain rat model was used. Paw withdrawal latency (PWL) was detected to evaluate the effects of celastrol on CFA-evoked inflammatory pain. After application of celastrol (1mg/kg, i.p.) on day 1, 3, 7 and 14 post-CFA injection, the expression levels of HMGB1, NF-κB, some proinflammatory markers, GFAP and CD11b in DRG were determined by qRT-PCR and western blot analysis. These results showed that celastrol significantly suppressed HMGB1, NF-κB and IL-1β mRNA and protein expression in DRG and alleviated CFA-evoked thermal hyperalgesia. Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-α, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. Collectively, the present study firstly provide evidences of the anti-inflammatory effect of celastrol via suppressing CFA-induced the activation of HMGB1/NF-κB signaling pathway in DRG, which maybe a potential therapeutic target for celastrol alleviating inflammatory pain.
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http://dx.doi.org/10.1016/j.neulet.2018.11.002DOI Listing
January 2019