Effect of Butylphthalide Capsules on Smac and XIAP Expression in Rats after Ischemia Reperfusion.

INTRODUCTION: Little is known about the protective effects of butylphthalide on cerebral ischemia-reperfusion injury. This study aims to investigate the impact on the second mitochondrial-derived activator of Caspases (Smac) and X-linked inhibitor of apoptosis protein (XIAP) expression in the ischemic semidark area using a rat model of carotid artery stenosis. METHODS: Thirty Sprague-Dawley rats were randomly divided into the sham-operated group, carotid stenosis model controls, low-dose (20 mg/kg), medium-dose (40 mg/kg), and high-dose (80 mg/kg) butylphthalide groups. The neurological function was scored by the balance beam test (BBT). The morphological changes of brain tissue were detected by Hematoxylin-eosin (HE) staining, with apoptosis detected by Terminal Deoxynucleotidyl Transferase mediated dUTP Nick-End Labeling (TUNEL) staining. Smac and XIAP protein expression were detected by immunohistochemistry (IHC). The expressions of Smac and XIAP mRNA were detected by real-time quantitative polymerase chain reaction (RT-qPCR). RESULTS: HE showed that neuronal loss, nuclear consolidation, and vacuolar degeneration were significantly reduced in the medium and high-dose butylphthalide groups compared with the model controls. The BBT scores and apoptotic index were significantly lower in the medium and high doses of butylphthalide compared with the model controls. RT-qPCR and IHC showed that Smac, XIAP mRNA and protein expressions in the ischemic hemispheric region were significantly reduced in low, medium, and high doses of butylphthalide compared with the model controls (P < 0.05), showing some concentration effect. CONCLUSIONS: Butylphthalide can significantly reduce Smac and XIAP mRNA and protein expression, inhibit neuronal apoptosis induced by ischemia-reperfusion injury in rats with carotid stenosis, and exert neuroprotective effects.

Effects of carbamazepine and sodium valproate on efficacy, cognitive function and uric acid in epileptic patients with first generalized seizure.

OBJECTIVE: To investigate the effects of carbamazepine and sodium valproate on efficacy, cognitive function and uric acid in epileptic patients with first generalized seizure. METHODS: 120 epilepsy patients with first generalized seizure who admitted to our hospital from March 2017 to March 2019, were selected and randomly divided into carbamazepine-group and sodium valproate-group, with 60 objects in each group. Both groups of patients received medication for one year. Subsequently, the changes in clinical efficacy, cognitive function, and blood uric acid of the two groups of patients 1 year after treatment were compared, and the correlation between blood uric acid and cognitive function was analyzed between the two groups. RESULTS: The two groups had statistically insignificant difference in the total effective rate (P>0.05). The cognitive function scores of the two groups after 6 months and 1 year of treatment were critically higher than those before treatment (P<0.05), and the comparison of cognitive function and blood uric acid degree between groups before treatment, 6 months after treatment and 1 year after treatment had statistically insignificant difference (P>0.05). There was a significant positive correlation between Mini-mental State Examination (MMSE) score of cognitive function and level of blood uric acid in patients with epilepsy (r=0.279, P=0.012). CONCLUSION: Both carbamazepine and valproate can effectively improve the cognitive function of patients with first generalized seizure, and the two medications have similar clinical efficacy. Patient's blood uric acid level increases after treatment, and there is a affirmative relationship between blood uric acid level and cognitive function of patients.

Effects of Different Degrees of Carotid Artery Stenosis on the Expression of XIAP and Smac in the Ischemic Penumbra of Rats with Cerebral Ischemia-Reperfusion.

OBJECTIVE: To investigate the effects of different degrees of carotid artery stenosis (CAS) on the expression of XIAP and Smac in ischemic penumbra of rats with cerebral ischemia-reperfusion (I/R). MATERIALS AND METHODS: Samples were collected at 12 h and 24 h after reperfusion, and then the treated groups were divided into the NC-12 group, NC-24 group, MIS-12 group, MIS-24 group, MOS-12 group, MOS-24 group, SES-12 group and SES-24 group. HE staining was used to observe the pathological changes of the brain tissue. TUNEL assay was used to detect the apoptosis in the ischemic penumbra. IHC and RT-qPCR were used to detect the expression of XIAP and Smac in the brain tissue. RESULTS: By observing the pathological sections of brain tissue, the rats in MIS, MOS and SES groups showed loose brain tissue on the infarcted side and neuronal pyknosis in the ischemic penumbra. And with the aggravation and prolongation of the degree of stenosis, the degree of brain injury deepened. It was further found that the TUNEL positive rate was significantly increased in the ischemic penumbra in the SES and MOS groups compared with that in the normal control (NC) group. The results of IHC and RT-qPCR showed that the mRNA expression of XIAP and Smac in the ischemic penumbra was significantly up-regulated in the MIS, MOS and SES groups compared with that in the NC group. CONCLUSIONS: CAS may activate XIAP/Smac signaling pathway to induce neuronal apoptosis and promote the injury in the ischemic penumbra caused by cerebral I/R.

Mutation detection in candidate genes for benign familial infantile seizures on a novel locus.

Benign familial infantile seizures (BFIS) is an autosomal dominant epileptic syndrome characterized by afebrile partial seizures with or without secondary generalized tonic-clonic seizures beginning at three to ten months of age. Genetic studies have revealed three susceptibility chromosomal loci on 19q12-q13.1, 16p12-q12 and 2q24. Previously we described the novel locus on 1p36.12-p35.1 for a Chinese family affected with BFIS, and below is a subsequent mutation analysis of candidate genes for the mapped chromosome region. Forty-five genes were selected and subjected to mutation analysis. Thirty-six nucleotide variants were found, none of which led to pathogenic changes, thereby were identified as nucleotide polymorphisms. The analyses suggest those candidate genes that were detected might not be involved in the epileptogenesis of pure BFIS, at least in the Chinese family we studied.