1.Curcumin stimulates proIiferation of rat neural stem cells by inhibiting glucocorticoid receptors
Xiaoxiao MA ; Chunman WANG ; Gaolong ZHANG ; Chunlong ZUO ; Yixiang HUANG ; Jin LLU ; Qingquan LLAN ; Han LLN
Chinese Journal of Pharmacology and Toxicology 2015;(2):202-207
OBJECTIVE To investigate the effect of curcumin on proliferation of neural stem cells (NSCs) of rats and the mechanism. METHODS NSCs derived from the forebrain of rat E15 embryos were cultured in vitro and identified by neuroepithelial stem cell protein ( nestin and SOX2) staining. NSCs were treated with curcumin 0.1, 0.5, 2.5, 12.5 and 62.5 μmol.L-1 for 24 h, respectively. The cyto-toxicity was estimated by measuring the release of lactate dehydrogenase(LDH). Cell viability and prolif-eration were analyzed respectively by MTT and BrdU assay. The mRNA expression levels of glucocorti-coid receptor (GR), Stat3, Notch1 and p21 were detected by qRT-PCR. The protein expression levels of total GR, Stat3 and phosphorylated Stat3 were measured by Western blotting. RESULTS The primary neural stem cells were identified as NSCs. Curcumin 12.5 and 62.5 μmol.L-1 had cell cytotoxicity( P<0.05). Cell viability assay indicated that curcumin 0.5 and 2.5 μmol.L-1 enhanced NSCs viability( P <0.05), but in 62.5 μmol.L-1 group the cell cytotoxicity was inhibited(P<0.05). Curcumin 0.1, 0.5 and 2.5 μmol.L-1 increased NSCs proliferation ( P < 0. 05), whereas 12. 5 and 62. 5 μmol.L-1 caused a decrease in NSCs proliferation(P<0.05). The mRNA expression level of GR in 0.5 μmol.L-1 group was significantly reduced( P<0.05). Western blotting analysis revealed that the protein expression of GR, Stat3 and p-Stat3 was inhibited by curcumin in 0.5 μmol.L-1 group(P<0.05). CONCLUSION Curcumin stimulates NSCs proliferation, possibly by inhibiting GR mRNA and related protein expression.
2.Guidelines on the Technical Plan for Emergency Health Response to Acute Gelsemium Poisoning
Jiaxin JIANG ; Ruibo MENG ; Zhongxiang GAO ; Rongzong LI ; Weifeng RONG ; Weihui LIANG ; Shibiao SU ; Jian HUANG ; Cheng JIN ; LlU XIAOYONG
China Occupational Medicine 2025;52(2):203-206
Acute Gelsemium poisoning is a systemic disease primarily affecting the central nervous system and respiratory symptoms caused by the ingestion of a substantial amount of Gelsemium within a short period. It manifests as sudden onset and rapid progression, primarily caused by accidental ingestion due to misidentification, and posing significant health risks. The compilation of the Technical Plan for Emergency Health Response to Acute Gelsemium Poisoning describes in detail the specialized practice and technical requirements in the process of handling acute Gelsemium poisoning, including accident investigation and management, laboratory testing and identification, in-hospital treatment, and health monitoring. The guidelines clarify key procedures and requirements such as personal protection, investigation elements, etiology determination, medical rescue, and health education. The key to acute Gelsemium poisoning investigation lies in promptly identifying the toxin through exposure history, clinical manifestations, and sample testing. Because there is no specific antidote for Gelsemium poisoning, immediate removal from exposure, rapid elimination of the toxin, and respiratory monitoring are critical on-site rescue measures. Visual identification of food or herbal materials, followed by laboratory testing to determine Gelsemium alkaloids in samples is a rapid effective screening method. These guidelines offer a scientific, objective, and practical framework to support effective emergency responses to acute Gelsemium poisoning incidences.