Objective To evaluate the effect of electroacupuncture (EA) preconditioning on the activity of dynamin-related protein 1 (Drp1) in brain tissues during cerebral ischemia-reperfusion (I/R) in rats.Methods A total of 126 pathogen-free healthy adult male Wistar rats,weighing 250-300 g,were divided into 3 groups (n =42 each) using a random number table:sham operation group (group S),group I/R and EA preconditioning group (group EA).In group S,the blood vessels were only separated but not occluded.In group I/R,a nylon thread with rounded tip was inserted into the left middle cerebral artery advanced cranially until resistance was met,and middle cerebral artery occlusion was maintained for 2 h followed by reperfusion.In group EA,Baihui acupoints were stimulated with an electric stimulator (2/ 15 Hz disperse-dense waves,intensity 1 mA) for 30 min,lasting for 5 consecutive days,and the model of focal cerebral I/R was established at 24 h after the last stimulation.At 6,24 and 48 h of reperfusion,the neurologic deficit was assessed and scored,the mitochondria in the cerebral cortex on the ischemic side were extracted,the expression of Drpl in mitochondria was detected using Western blot,the mitochondrial uhrastructure was examined with an electron microscope,and neuroapoptosis was measured using TUNEL.The apoptosis rate was calculated.Results Compared with group S,the neurological deficit score and apoptosis rate were significantly increased,and the expression of Drpl in mitochondria was up-regulated at each time point in I/R and EA groups (P＜0.05).Compared with group I/R,the neurological deficit score and apoptosis rate were significantly decreased,and the expression of Drpl in mitochondria was down-regulated at each time point in group EA (P＜0.05).Conclusion The mechanism by which EA preconditioning reduces cerebral I/R injury may be related to inhibiting the activity of Drpl and thus inhibiting the excessive fission of mitochondria in rats.

Objective To evaluate the effect of electroacupuncture (EA) preconditioning on inositol-requiring kinase 1 (IRE1)-X-box binding protein 1 (XBP1) signaling pathway in endoplasmic reticulum in the cortex in a rat model of cerebral ischemia-reperfusion (I/R).Methods One hundred and eight pathogen-free healthy male Sprague-Dawley rats,aged 8-12 weeks,weighing 200-250 g,were assigned into 3 groups (n =36 each) using a random number table:sham operation group (group S),group I/R and EA preconditioning group (group EA).Focal cerebral I/R was induced by occlusion of right middle cerebral arteries for 2 h followed by reperfusion in rats anesthetized with chloral hydrate.In group EA,Baihui acupoints were stimulated with an electric stimulator for 30 min once a day for 5 consecutive days starting from 5 days before ischemia,and the model was established at 24 h after the last preconditioning.Rats were sacrificed after neurological deficit was scored at 6,12 and 24 h of reperfusion,brains were removed,and the ischemic area in cerebral cortex was isolated for examination of the cell ultrastructure (with an electronic microscope) and for determination of the expression of IRE1 and XBP1 (by Western blot).Results Compared with group S,the neurological deficit scores were significantly increased,and the expression of IRE1 and XBP1 in the ischemic area was up-regulated at each time point in I/R and EA groups (P＜0.01).Compared with group I/R,the neurological deficit scores were significantly decreased,and the expression of IRE1 and XBP1 was up-regulated at each time point in group EA (P＜0.05).The cell damage in the ischemic area in cerebral cortex was significantly attenuated in group EA when compared with group I/R.Conclusion The mechanism by which EA preconditioning attenuates cerebral I/R injury is related to activating IRE1-XBP 1 signaling pathway and relieving endoplasmic reticulum stress in rats.

Objective:To investigate the clinical and genetic features in a family with type 2 congenital generalized lipodystrophy, and to improve the understanging of this disease.Methods:The clinical symptoms, results of the laboratory, and radiography examinations of the patient and his family members were analyzed. The whole exome sequencing and Sanger validation were used to determine the genetic cause of the disease.Results:Generalized lipodystrophy, impaired liver function, severe hypertriglyceridemia, and acanthosis nigricans were found in the proband. His serum leptin level was much lower than normal value. The proband and three members of this family were confirmed to have insertion mutation at exon 5 of BSCL2 gene. The site was mutated from TTC to TCGGTC, resulting in the replacement of glutamate by aspartate and arginine. The mutation in proband was homozygote, and his father, mother, and brother were heterozygous.Conclusions:The mutation in exon 5 c. 545_546insCCG of BSCL2 gene leads to the occurrence of type 2 congenital generalized lipodystrophy.