Electroacupuncture improves learning and memory functions in a rat cerebral ischemia/reperfusion injury model through PI3K/Akt signaling pathway activation.

Electroacupuncture has been widely used to treat cognitive impairment after cerebral ischemia, but the underlying mechanism has not yet been fully elucidated. Studies have shown that autophagy plays an important role in the formation and development of cognitive impairment, and the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway plays an important role in autophagy regulation. To investigate the role played by the PI3K/Akt signaling pathway in the electroacupuncture treatment of cerebral ischemia/reperfusion rat models, we first established a rat model of cerebral ischemia/reperfusion through the occlusion of the middle cerebral artery using the suture method. Starting at 2 hours after modeling, electroacupuncture was delivered at the Shenting (GV24) and Baihui (GV20) acupoints, with a dilatational wave (1-20 Hz frequency, 2 mA intensity, 6 V peak voltage), for 30 minutes/day over 8 consecutive days. Our results showed that electroacupuncture reduced the infarct volume in a rat model of cerebral ischemia/reperfusion injury, increased the mRNA expression levels of the PI3K/Akt signaling pathway-related factors Beclin-1, mammalian target of rapamycin (mTOR), and PI3K, increased the protein expression levels of phosphorylated Akt, Beclin-1, PI3K, and mTOR in the ischemic cerebral cortex, and simultaneously reduced p53 mRNA and protein expression levels. In the Morris water maze test, the latency to find the hidden platform was significantly shortened among rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation. In the spatial probe test, the number of times that a rat crossed the target quadrant was increased in rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation. Electroacupuncture stimulation applied to the Shenting (GV24) and Baihui (GV20) acupoints activated the PI3K/Akt signaling pathway and improved rat learning and memory impairment. This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, China (approval No. 8150150901) on March 10, 2016.

[Morphological and histological studies of Herpetospermum pedunculosum seeds and other substitutes].

OBJECTIVE: To provide new evidences for the identification of Herpetospermum pedunculosum seeds and other substitutes. METHOD: Microscopic examination of the cross sections and powers of the seeds of H. pedunculosum, Momordica charantia, Thladiantha setispina and M. cohinchinensis were made to characterize the drug materials. RESULT AND CONCLUSION: The external and internal structure of T. setispina and M. charantia were studied for the first time. Two types of different branched starry sclereids was found in M. cohinchinensis. Comparative studies on external and internal structure were carried out on seeds of the 4 species. As a result, they could be distinguished by external characteristics such as shape, size and color of their seeds, and by internal structure such as size and type of sclereid, epidermis and sub-epidermis cell of seed coat.

Swietenia mahagony extract shows agonistic activity to PPAR(gamma) and gives ameliorative effects on diabetic db/db mice.

AIM: To search the peroxisome proliferator-activated receptor g (PPAR(gamma)) agonists from Swietenia mahagony extract (SmE) and observe the possible ameliorative effects of SmE on diabetic db/db mice. METHODS: The PPAR(gamma) agonistic activity of SmE was screened by yeast-two hybrid system. The blood glucose levels of diabetic db/db mice were measured using a blood glucose level monitor and the data were statistically analyzed by NDST8.8W software. RESULTS: By using the clinical drug rosiglitazone as a positive control, it was found that the PPARg agonistic activity of SmE at a concentration of 50 microg/L was approximately half that of 35.7 microg/L (0.1 micromol/L) of rosiglitazone. At the dose of 1000 mg/kg, SmE remarkably decreased the blood glucose concentration of db/db mice from (15.26+/-2.98) to (7.58+/-2.20) mmol/L, and reduced the blood glucose levels by 55.49% compared with the control group (P<0.01). CONCLUSION: SmE shows agonistic activity to PPARg and can ameliorate the blood glucose levels of diabetic db/db mice. SmE may be thus used as a potential agent for diabetes therapy.