Neural Regen Res
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Antenatal administration of magnesium sulfate is an important part of the neuroprotective strategy for preterm infants. Strong evidence from five randomized controlled trials and five meta-analyses has demonstrated that magnesium sulfate, when administered before preterm delivery, significantly reduces the risk of cerebral palsy at two years. ⋯ Since 2010, an increasing number of obstetrical societies have recommended its use to improve the neurological outcomes of preterm infants, especially the International Federation of Gynecology and Obstetrics and World Health Organization in 2015, and France in 2017. Considering the neuroprotective impact of magnesium sulfate when administered before delivery, postnatal administration should be considered, and its effects should be assessed using randomized controlled trials.
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Rosmarinic acid (RA) can elicit a neuroprotective effect against ischemic stroke, but the precise molecular mechanism remains poorly understood. In this study, an experimental ischemic stroke model was established in CD-1 mice (Beijing Vital River Laboratory Animal Technology, Beijing, China) by occluding the right middle cerebral artery for 1 hour and allowing reperfusion for 24 hours. After intraperitoneally injecting model mice with 10, 20, or 40 mg/kg RA, functional neurological deficits were evaluated using modified Longa scores. ⋯ However, intraperitoneal injection of a HO-1 inhibitor (10 mg/kg zinc protoporphyrin IX) reversed the neuroprotective effects of RA on HO-1 enzyme activity and Bcl-2 and Bax protein expression. The PI3K/Akt signaling pathway inhibitor LY294002 (10 mM) inhibited Akt phosphorylation, as well as Nrf2 and HO-1 expression. Our findings suggest that RA has anti-oxidative and anti-apoptotic properties that protect against ischemic stroke by a mechanism involving upregulation of Nrf2 and HO-1 expression via the PI3K/Akt signaling pathway.
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Contralateral C7 (cC7) root transfer to the healthy side is the main method for the treatment of brachial plexus root injury. A relatively new modification of this method involves cC7 root transfer to the lower trunk via the prespinal route. In the current study, we examined the effectiveness of this method using electrophysiological and histological analyses. ⋯ Toluidine blue staining was used to count the number of myelinated nerve fibers in the injured nerves. Compared with the traditional method, cC7 root transfer to the lower trunk via the prespinal route increased grasp strength of the injured forepaw, increased the compound muscle action potential maximum amplitude, shortened latency, substantially restored tetanic contraction of the forearm flexor muscles, increased the wet weight of the muscle, reduced atrophy of the flexor digitorum superficialis muscle, and increased the number of myelinated nerve fibers. These findings demonstrate that for finger flexion functional recovery in rats with total brachial plexus injury, transfer of the cC7 root to the lower trunk via the prespinal route is more effective than transfer to the median nerve via subcutaneous tunnel.
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Long non-coding RNAs regulate brain microvascular endothelial cell death, the inflammatory response and angiogenesis during and after ischemia/reperfusion and oxygen-glucose deprivation/reoxygenation (OGD/R) insults. The long non-coding RNA, SNHG12, is upregulated after ischemia/reperfusion and OGD/R in microvascular endothelial cells of the mouse brain. However, its role in ischemic stroke has not been studied. ⋯ After exposure to OGD for 16 hours, these cells were then analyzed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, trypan blue exclusion, western blot, and capillary-like tube formation assays. Overexpression of SNHG12 inhibited brain microvascular endothelial cell death and the inflammatory response but promoted angiogenesis after OGD/R, while SNHG12 knockdown had the opposite effects. miR-199a was identified as a target of SNHG12, and SNHG12 overexpression reversed the effect of miR-199a on brain microvascular endothelial cell death, the inflammatory response, and angiogenesis. These findings suggest that SNHG12 suppresses endothelial cell injury induced by OGD/R by targeting miR-199a.
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Post-stroke spasticity is associated with restriction in the range of motion of the shoulder. Reducing muscular dystrophy may help relieve muscular dysfunction in patients with post-stroke shoulder spasticity. Dry needle therapy is a method of needling the trigger points using a syringe needle without the use of a drug. ⋯ After the first and ninth treatment, the Modified Ashworth Scale and the passive range of motion of the shoulder was used to assess the effect of the treatment. The spasticity and range of motion of the shoulder showed obvious improvement. These results indicate that dry needling at the myofascial trigger points can effectively treat chronic post-stroke shoulder spasticity.