Study on the Optimum Picking Time of Callicarpa kwangtungensis

[Objective] This study was conducted to compare total contents of poliumoside and forsythoside B from Callicarpa kwangtungensis Chun in Qiandongnan Miao and Dong Autonomous Prefecture collected in different seasons, which could provide reference for its deep development and utilization. [Methods] Poliumoside and forsythoside B were measured according to the pharmacopoeia standard in the middle of each month in 2014, and the yield of C. kwangtungensis was simultaneously evaluated. All these results provided data reference for the determination of suitable picking time for C. kwangtungensis. [Results] The results showed the content of poliumoside and forsythoside B in C. kwangtungensis was the highest in November, and the content of the medicinal material in August was over eight times higher than the pharmacopoeia standard, besides at this month the yield was the highest during the year. Comprehensively, mid October is the optimum picking time for C. kwangtungensis in Taijiang. [Conclusion] Dynamic variations of content of poliumoside and forsythoside B in and yield of C. kwangtungensis were investigated, which would significantly benefit production of C. kwangtungensis in Qiandongnan Miao and Dong Autonomous Prefecture.

Inhibition of intracellular proton-sensitive Ca^(2+)-permeable TRPV3 channels protects against ischemic brain injury

Ischemic brain stroke is pathologically characterized by tissue acidosis, sustained calcium entry and progressive cell death. Previous studies focusing on antagonizing N-methyl-D-aspartate(NMDA) receptors have failed to translate any clinical benefits, suggesting a non-NMDA mechanism involved in the sustained injury after stroke. Here, we report that inhibition of intracellular proton-sensitive Ca^(2+)-permeable transient receptor potential vanilloid 3(TRPV3) channel protects against cerebral ischemia/reperfusion(I/R) injury. TRPV3 expression is upregulated in mice subjected to cerebral I/R injury. Silencing of TRPV3 reduces intrinsic neuronal excitability, excitatory synaptic transmissions, and also attenuates cerebral I/R injury in mouse model of transient middle cerebral artery occlusion(tMCAO). Conversely, overexpressing or re-expressing TRPV3 increases neuronal excitability, excitatory synaptic transmissions and aggravates cerebral I/R injury. Furthermore, specific inhibition of TRPV3 by natural forsythoside B decreases neural excitability and attenuates cerebral I/R injury. Taken together, our findings for the first time reveal a causative role of neuronal TRPV3 channel in progressive cell death after stroke, and blocking overactive TRPV3 channel may provide therapeutic potential for ischemic brain injury.