Objective:To investigate the effects of glimepiride on cerebral edema and apoptosis in a rat model of sub-arachnoid hemorrhage(SAH).Methods:An SAH model was established in rats using the internal carotid artery punc-ture method.Low-dose glimepiride was administered via intraperitoneal injection.Neurological deficits were assessed u-sing the modified Neurological Severity Score(mNSS),and brain water content was evaluated by measuring the wet-dry weight ratio of brain tissue.Cortical tissue from the surgical side was collected to measure the mRNA expression of sul-fonylurea receptor 1(SUR1)and transient receptor potential melastatin 4(TRPM4)using RT-qPCR,while the protein expression of Bcl-2 and Bax was detected by Western blot.Results:SAH rats exhibited impaired neurological function,increased brain water content,upregulation of SUR1 and TRPM4 mRNA expression,and a decreased Bcl-2/Bax ratio.Low-dose glimepiride did not affect blood glucose levels but significantly improved neurological function and reduced cerebral edema in SAH rats.Although glimepiride had no significant effect on SUR1 and TRPM4 mRNA expression,it increased the Bcl-2/Bax ratio.Conclusion:Glimepiride alleviates cerebral edema and inhibits apoptosis in SAH model rats by suppressing the SUR1-TRPM4 channel.

Adolescent idiopathic scoliosis(AIS)is a complex three-dimensional deformity involving coronal,sagittal,and axial planes,with a prevalence that should not be overlooked.With advancements in technology and in-depth research,an increasing number of hospitals and physicians are exploring standardized diagnostic and treatment approaches for AIS.Comprehensive and in-depth understanding is required for AIS,including its etiology,screening and diagnosis,classification,assessment and examination,treatment options,exploration of current focus,and evaluation of quality of life.Such understanding ensures that the diagnostic and treatment are scientific,standardized,and timely.Based on the principles of evidence-based medicine,a consensus on the diagnosis and treatment of AIS is reached after multiple discussions among spinal surgery experts,aiming to provide reference and guidance for clinical practice.

Objective:To explore the effect of melatonin on mitophagy in the brain tissue of rats with early subarach-noid hemorrhage(SAH).Methods:The rat model of SAH was established by internal carotid artery puncture and trea-ted with melatonin by intraperitoneal injection.At 24 hours after the operation,the neurological function of rats was de-tected by mNSS score and balance beam test.The contents of reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)and in brain tissue were detected by commercial reagent kits.The expression changes of PINK1/Parkin,microtubule-associated protein1A/1B-light chain3(LC3)and p62 in brain tissue were detected by Western blot.Results:Melatonin can significantly improve the neurological function of SAH rats,reduce the con-tents of MDA(P<0.05)and ROS(P<0.05),and increase the content of GSH(P<0.05).Meanwhile,Western blot detection indicated that melatonin could increase the expression of PINK1 and Parkin(P<0.05),increase the ratio of LC3-II/LC3-I(P<0.05),and reduce the expression of p62(P<0.05).Conclusion:Melatonin alleviates early brain injury in rats with subarachnoid hemorrhage through PINK1/Parkin-mediated mitophagy.

Objective:To evaluate the effect of deep brain stimulation(DBS)of the lateral cerebellar nucleus(LCN)on synaptic plasticity in a traumatic brain injury(TBI)rat model of the medial prefrontal cortex(mPFC).Methods:A controllable mPFC injury rat model was prepared using a hydraulic impact method.Two weeks after inju-ry,stimulation electrodes were implanted into the left LCN.Electrical stimulation was initiated at the 4th week after injury and continued for 30 days.The learning and memory function of the rats was evaluated using the Morris water maze.RT-qPCR and Western blot were used to detect the mRNA and protein expressions of brain-derived neurotrophic factor(BDNF),postsynaptic density protein 95(PSD95),and growth-associated protein 43(GAP43)in the mPFC region.Results:The learning and memory function of the mPFC-injured rats significantly decreased.The expressions of BDNF,PSD95,and GAP43 in mPFC decreased.DBS treatment significantly enhanced the learning and memory ability of mPFC-injured rats,and simultaneously upregulated the expressions of BDNF,PSD95,and GAP43 in mPFC.Conclusion:LCN DBS is an effective method for treating cognitive impairment caused by TBI,and it may achieve this through activating the neural plasticity mechanism of the mPFC.

Objective:To evaluate the effect of deep brain stimulation(DBS)of the lateral cerebellar nucleus(LCN)on synaptic plasticity in a traumatic brain injury(TBI)rat model of the medial prefrontal cortex(mPFC).Methods:A controllable mPFC injury rat model was prepared using a hydraulic impact method.Two weeks after inju-ry,stimulation electrodes were implanted into the left LCN.Electrical stimulation was initiated at the 4th week after injury and continued for 30 days.The learning and memory function of the rats was evaluated using the Morris water maze.RT-qPCR and Western blot were used to detect the mRNA and protein expressions of brain-derived neurotrophic factor(BDNF),postsynaptic density protein 95(PSD95),and growth-associated protein 43(GAP43)in the mPFC region.Results:The learning and memory function of the mPFC-injured rats significantly decreased.The expressions of BDNF,PSD95,and GAP43 in mPFC decreased.DBS treatment significantly enhanced the learning and memory ability of mPFC-injured rats,and simultaneously upregulated the expressions of BDNF,PSD95,and GAP43 in mPFC.Conclusion:LCN DBS is an effective method for treating cognitive impairment caused by TBI,and it may achieve this through activating the neural plasticity mechanism of the mPFC.

Objective:To investigate the effects of glimepiride on cerebral edema and apoptosis in a rat model of sub-arachnoid hemorrhage(SAH).Methods:An SAH model was established in rats using the internal carotid artery punc-ture method.Low-dose glimepiride was administered via intraperitoneal injection.Neurological deficits were assessed u-sing the modified Neurological Severity Score(mNSS),and brain water content was evaluated by measuring the wet-dry weight ratio of brain tissue.Cortical tissue from the surgical side was collected to measure the mRNA expression of sul-fonylurea receptor 1(SUR1)and transient receptor potential melastatin 4(TRPM4)using RT-qPCR,while the protein expression of Bcl-2 and Bax was detected by Western blot.Results:SAH rats exhibited impaired neurological function,increased brain water content,upregulation of SUR1 and TRPM4 mRNA expression,and a decreased Bcl-2/Bax ratio.Low-dose glimepiride did not affect blood glucose levels but significantly improved neurological function and reduced cerebral edema in SAH rats.Although glimepiride had no significant effect on SUR1 and TRPM4 mRNA expression,it increased the Bcl-2/Bax ratio.Conclusion:Glimepiride alleviates cerebral edema and inhibits apoptosis in SAH model rats by suppressing the SUR1-TRPM4 channel.

Objective:To explore the effect of melatonin on mitophagy in the brain tissue of rats with early subarach-noid hemorrhage(SAH).Methods:The rat model of SAH was established by internal carotid artery puncture and trea-ted with melatonin by intraperitoneal injection.At 24 hours after the operation,the neurological function of rats was de-tected by mNSS score and balance beam test.The contents of reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)and in brain tissue were detected by commercial reagent kits.The expression changes of PINK1/Parkin,microtubule-associated protein1A/1B-light chain3(LC3)and p62 in brain tissue were detected by Western blot.Results:Melatonin can significantly improve the neurological function of SAH rats,reduce the con-tents of MDA(P<0.05)and ROS(P<0.05),and increase the content of GSH(P<0.05).Meanwhile,Western blot detection indicated that melatonin could increase the expression of PINK1 and Parkin(P<0.05),increase the ratio of LC3-II/LC3-I(P<0.05),and reduce the expression of p62(P<0.05).Conclusion:Melatonin alleviates early brain injury in rats with subarachnoid hemorrhage through PINK1/Parkin-mediated mitophagy.

Objective:Osteopontin(OPN)has demonstrated neuroprotective effects in various stroke models.Its role in neuroinflammation after brain injury remains to be elucidated.This study aims to clarify the effect of OPN on neuroin-flammation,particularly on the functional states of microglia after subarachnoid hemorrhage(SAH).Methods:Thirty rats were randomly divided into the following groups:Sham,SAH,and SAH+OPN.SAH rat model was prepared by secondary injection of autologous arterial blood,and OPN was given intranasally in the treatment group.Neurological function was evaluated by modified Garcia score.The degree of cerebral edema was evaluated by measuring brain water content.The expression of microglia activation markers CD86,inducable nitric oxide synthase(iNOS),CD206 and arginase 1(Arg-1)after SAH and OPN treatment was detected by RT-qPCR.The levels of IL-1β,IL-6,IL-10,and IL-13 in cerebrospinal fluid were detected by enzyme-linked immunosorbent assay(ELISA).Results:Intranasal ad-ministration of OPN could improve the neurological dysfunction and cerebral edema in SAH rats.What's more,OPN could inhibit the expression of CD86,iNOS,IL-1β,and IL-6 in cerebral while promote the expression of CD206,Arg-1,IL-10,and IL-13.Conclusion:OPN alleviates the inflammatory response after SAH by inhibiting the polarization of microglia M1.

Objective:To study the role of DDX3X/NF-κB pathway in early neuronal apoptosis in subarachnoid hemorrhage(SAH)mice.Methods:The mouse model of SAH was established by internal carotid artery puncture,and the neurological function score of the mice was evaluated.The DDX3X expression was knocked down using recombinant lentivirus expressing DDX3X targeted shRNA(Lv-shDDX3X),or the NF-κB pathway was inhibited by NF-κB-IN-1(IN-1).Western Blot was used to detect the expression of DDX3X and NF-κB(p65)in mouse cortex.TUNEL/NeuN staining was used to detect the apoptosis of cerebral cortex neurons.Results:Twenty-four hours after SAH operation,the neurological function of mice was significantly impaired(P＜0.05).While the expression of DDX3X was signifi-cantly increased and the expression of NF-κB(p65)was significantly decreased in the cortex(P＜0.05).When the DDX3X expression is knocked down firstly,then SAH surgery is performed.The neurological function of mice was sig-nificantly recovered,and the expression of NF-κB(p65)protein was significantly higher than that in SAH group(P＜0.05);If the NF-κB activity was inhibited by IN-1 while DDX3X knockdown,there is no significant recovery of neuro-logical function in SAH mice.TUNEL/NeuN staining showed that the number of TUNEL-positive neurons in the brain tissue after DDX3X knockdown was less than that in the SAH group(P＜0.05),while the number of TUNEL-positive neurons was not significantly reduced when IN-1 was used to inhibit NF-κB activity at the same time of DDX3X knock-down.Conclusion:DDX3X/NF-κB mediated cell death in mice with early brain injury after SAH.

Objective:Cerebral hemorrhage can lead to neuronal cell death,nervous system disorder and permanent disability.Chlorogenic acid(CGA)has antioxidant,anti-inflammatory and anti-apoptotic properties.This study was to investigate the neuroprotective effect of CGA on subarachnoid hemorrhage(SAH)in rats.Methods:SAH was induced by carotid artery puncture in male adult rats.CGA(30 mg/kg)was injected intraperitoneally 2 h after SAH.Neurologi-cal outcomes were assessed 24 h after SAH by modified Garcia scores and the beam balance test.The brain edema was evaluated by dry-wet ratio method.Oxidative stress was assessed by measuring reactive oxygen species(ROS)and su-peroxide dismutase(SOD)activity in rat cortex using commercial kits.Results:SAH caused severe neurobehavioral defects and cerebral edema in rats.The level of ROS in cerebral cortex increased,while the activity of SOD decreased.However,CGA treatment improved the neurobehavioral deficits induced by SAH,while reducing ROS levels and enhan-cing SOD activity.Conclusion:CGA plays a neuroprotective role through anti-oxidative stress.