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1.
Chinese Journal of Cellular and Molecular Immunology ; (12): 410-415, 2023.
Artigo em Chinês | WPRIM | ID: wpr-981881

RESUMO

Objective To investigate the protective effect of artesunate on hypoxic-ischemic brain damage (HIBD) and its mechanism in neonatal rats. Methods 7-day-old neonatal SD rats were randomly divided into sham operation group, model group, artesunate 5 mg/kg group, artesunate 10 mg/kg group, artesunate 20 mg/kg group and dexamethasone 6 mg/kg group, with 18 rats in each group. HIBD models were established in groups except for the sham operation group. The sham operation group only needed to separate the left common carotid artery without ligation and nitrogen-oxygen mixed gas ventilation. Each group was injected with drug intraperitoneally right after surgery and the rats in the sham operation group and the model group were injected with an equal volume of normal saline (once a day for a total of 5 times). One hour after the last injection, the rats in each group were scored for neurological defects. After the rats were sacrificed, the brain water content was measured and the pathological changes of the brain tissues of rats were observed. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) was used to detect the neuronal cell apoptosis, and ELISA was applied to detect the levels of IL-1β, IL-6 and TNF-α in brain tissues and peripheral blood of each group of rats. Western blot analysis was adopted to detect the protein expression levels of NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing CARD (ASC) and caspase-1 in the rats brain tissues of each group. Results Compared with the model group, the neurological deficit score was decreased; the pathological damage of brain tissues was relieved; the brain water content was significantly reduced; the apoptosis number of hippocampal neurons was decreased significantly; the levels of IL-1β, IL-6 and TNF-α in brain tissues and peripheral blood were significantly reduced; the protein expression levels of NLRP3, ASC and caspase-1 were significantly lowered in the middle-dose and high-dose artesunate groups and the dexamethasone group. Conclusion Artesunate can improve the neurological function, relieve the brain damage, and alleviate the brain edema in neonatal rats with HIBD. It can protect the HIBD, which may be related to the inhibition of NLRP3 inflammasome activation and reduction of inflammatory cytokine secretion.


Assuntos
Animais , Ratos , Animais Recém-Nascidos , Artesunato/farmacologia , Encéfalo/metabolismo , Caspases/metabolismo , Dexametasona , Hipóxia-Isquemia Encefálica/patologia , Inflamassomos , Interleucina-6/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa/metabolismo , Água/metabolismo
2.
Chinese Journal of Applied Clinical Pediatrics ; (24): 1672-1674, 2020.
Artigo em Chinês | WPRIM | ID: wpr-864297

RESUMO

Objective:To improve recognition of the clinical phenotype and genotype of achondroplasia(ACH).Methods:The clinical data and genetic test results of 2 children with ACH were analyzed retrospectively, and the related literature was reviewed.Results:Case 1 was a 1-year-old girl whose mother was short in stature.She was admitted to the hospital due to knee reflexes of both lower limbs for more than 9 months.Physical examination showed that her head circumference was 45 cm and she had short stature, short limbs, low muscle tension of both lower limbs, the developmental quotient was 65 scores.Bilateral ilium and hip joint lesions by X-ray were considered as ACH.According to the submitted gene results, FGFR3 gene c. 1138G >A (p.Gly380Arg) of the girl showed the heterozygous variation, and that gene of her mother showed the heterozygous variation.Case 2 was a 10-month-old girl, who was admitted to the hospital due to limb weakness for over 5 months.Physical examination showed head circumference of 46 cm, short stature, short limbs, reduced muscle tension of limbs, grade 4 muscle strength of limbs, and the developmental quotient was 41 scores.X-ray showed that both lower limbs were in accordance with ACH.The gene results suggested the heterozygous variation of FGFR3 gene c. 1138G >A (p.Gly380Arg) in the girl(a novel mutation), and a wild-type gene in her parents. Conclusions:The clinical features of achondroplasia are diverse.The bone changes and nerve development also need to be recognized and discriminated.

3.
Chinese Journal of Applied Clinical Pediatrics ; (24): 1506-1508, 2020.
Artigo em Chinês | WPRIM | ID: wpr-864251

RESUMO

Objective:To improve the recognition of clinical phenotype and genotype of Angelman syndrome(AS).Methods:The clinical data of a child with AS in Department of Pediatric Rehabilitation, the First Affiliated Hospital of Xinxiang Medical University at May 2018 was analyzed, retrospectively.Results:One 2- year-old female child could not walk alone for more than half a year.The physical examination proved that her head circumference was small, speech was unable, gait was unstable and the toes and feet were pointed.The developmental quotient was 19 points; the motor score was 10 points and the language score was 7 points.The c. 580G>T heterozygous nonsense variation of UBE3A gene was discovered through whole exon sequencing.This mutation resulted in the termination of amino acid 194 Glu(p.Glu194Stop, 682), which was nonsense variation, making the protein lose 682 amino acids.Family verification proved that c. 580G>T was a novel variant, and both parents were wild type. Conclusion:It is obvious that the heterozygous nonsense mutation of UBE3A gene c. 580G>T is a new cause of AS.

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