Objective: To examine the relationship between traditional Chinese medicine (TCM) constitutional types and health status among groups of different age or gender in the general population of China. Methods: Data of 8 448 cases were randomly sampled from a database of 21 948 cases of a cross-sectional survey on the TCM constitutional types and health status which was carried out in 9 provinces or municipalities of China (Jiangsu, Anhui, Gansu, Qinghai, Fujian, Beijing, Jilin, Jiangxi and Henan) according to gender and age structure of the Chinese population in 2005. Scores of health-related quality of life scale--the Medical Outcomes Study 36-Item Short-Form Health Survey (MOS SF-36)--were analyzed by Nemenyi test to compare the health status of individuals with different constitutional types. Results: Compared with the gentleness type, the MOS SF-36 scores of the 8 types of pathological constitution were significantly low (P<0.05) among groups of different age or gender. The MOS SF-36 score was the lowest in men of the qi-deficiency, qi-depression and blood-stasis types, while it was the lowest in women of the phlegm-dampness, qi-depression and qi-deficiency types. For the age group of 15 to 34, the special diathesis, qi-depression and blood-stasis types had the lowest MOS SF-36 scores; for the age group of 35 to 59, the qi-deficiency, qi-depression and blood-stasis types had the lowest MOS SF-36 scores; for the age group of over 60, the qi-deficiency, qi-depression and phlegm-dampness types had the lowest MOS SF-36 scores. Conclusion: In groups of different gender or age, the MOS SF-36 scores of the 8 types of pathological constitution were significantly lower than that of the gentleness type, indicating a deficient health status. The health status of different types of constitution showed different characteristics in groups of different gender or age.

Objective:To evaluate the role of protein O-linked beta-N-acetylglucosaminylation (O-GlcNAcylation) modification in oxidative stress injury in nerve cells of mice subjected to oxygen-glucose deprivation and restoration (OGD/R).Methods:The standard mouse hippocampal neuron cell line was inoculated on a culture plate or dish at a density of 5×10 4 cells/ml and divided into 4 groups ( n=20 each) using a random number table method: normal group (N group), O-(connection)N-acetylglucosamine hydrolase (OGA) inhibitor Thiamet G group (T group), OGD/R group (D/R group) and Thiamet G+ OGD/R complex sugar group (T-D/R group). The cells were exposed to a mixed gas of 94% N 2-5% CO 2-1% O 2 for 6 h in a low-glucose medium, then medium was replaced with a common medium for restoring oxygen and glucose, and the cells were cultured for 12 h. Thiamet G at a final concentration of 1 mmol/L was added to the culture medium at 4 h before OGD/R in T-D/R group, and the medium was replaced with a medium containing Thiamet G at a final concentration of 1 mmol/L at 4 h before extraction of cellular proteins.After oxygen and glucose restoration was completed, the accumulation of cellular ROS was measured using DCFH-DA staining, mitochondrial membrane potential was measured using Jc-1 staining, O-GlcNAc modification was determined by immunofluorescence, and the expression of nuclear factor E2-related factor 2 (Nrf2), c-Jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK), and p53 tumor suppressor gene (p53) was detected using Western blot. Results:Compared with group N, the expression of O-GlcNAc in nerve cells was significantly up-regulated in group T, and the accumulation of ROS in nerve cells was significantly increased, JC-1 monomer was increased, JC-1 polymer was decreased, Nrf2 expression was down-regulated, and the expression of p-JNK and p53 was up-regulated in group D/R, and the expression of O-GlcNAc in nerve cells was up-regulated, the accumulation of ROS was increased, the polymerization of JC-1 monomer and JC-1 was increased, Nrf2 expression was down-regulated, and the expression of p-JNK and p53 was up-regulated in group T-D/R ( P<0.05). Compared with group D/R, the expression of O-GlcNAc in nerve cells was significantly up-regulated, the accumulation of ROS was decreased, JC-1 monomer was decreased, JC-1 polymer was increased, the expression of Nrf2 was up-regulated, and the expression of p-JNK and p53 was down-regulated in group T-D/R ( P<0.05). Conclusion:When mouse nerve cells are subjected to OGD/R, the protein O-GlcNAc modification as an endogenous protective mechanism is enhanced, which can reduce oxidative stress injury, and the mechanism may be related to regulating the Nrf2-mediated JNK pathway.

Objective:To evaluate the relationship between silence information regulator 1 (SIRT1) and signal transducers and activators of transcription 3 (STAT3) acetylation during high glucose-induced cardiac microvascular endothelial cell injury.Methods:Cardiac microvascular endothelial cells of Sprague-Dawley rats were cultured.The cells at the logarithmic growth phase were selected and divided into 3 groups ( n=24 each) using a random number table method: control group (C group), high glucose group (HG group) and high glucose+ SIRT1 agonist SRT1720 group (HG+ SRT group). The cardiac microvascular endothelial cells were seeded in a 6- or 96-well cell culture plate at a density of 2×10 5 cells/ml.When the cell density reached 50%, the culture medium was then replaced with high-glucose (glucose 33 mmol/L) DMEM culture medium containing with 10% fetal bovine serum and 1% double antibody in HG and HG+ SRT groups.In group HG+ SRT, 20 μmol/L SRT1720 was added simultaneously, and the cells were cultured at 37 ℃ in an incubator with 5% CO 2 for 24 h. The cell viability was determined by CCK-8 assay, the activity of superoxide dismutase (SOD) was detected using a spectrophotometer, the levels of lactic dehydrogenase (LDH), interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) in the supernatant were detected by enzyme-linked immunosorbent assay, and the expression of SIRT1, acetylated STAT3 (ac-STAT3) and phosphorylated STAT3 (p-STAT3) was determined by Western blot. Results:Compared with C group, the cell viability and SOD activity were significantly decreased, levels of LDH, IL-6 and TNF-β in the supernatant were increased, expression of SIRT1 was down-regulated, and expression of ac-STAT3 and p-STAT3 was up-regulated in group HG and group HG+ SRT ( P<0.05). Compared with group HG, the cell viability and SOD activity were significantly increased, levels of LDH, IL-6 and TNF-β in the supernatant were decreased, expression of SIRT1 was up-regulated, and expression of ac-STAT3 and p-STAT3 was down-regulated in group HG+ SRT ( P<0.05). Conclusion:SIRT1 can alleviate high glucose-induced cardiac microvascular endothelial cell injury by promoting STAT3 deacetylation.

Objective:To evaluate the relationship between protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway-mediated endoplasmic reticulum stress and the reduction of cerebral ischemia-reperfusion (I/R) injury by dexmedetomidine in mice by the in vivo experiment and the cell experiment. Methods:In the in vivo experiment, 20 healthy clean-grade male mice, aged 6-8 weeks, weighing 20-30 g, were divided into 4 groups ( n=5 each) using a random number table method: sham operation group (group S), sham operation+ dexmedetomidine group (group SD), cerebral I/R group (group IR) and cerebral I/R+ dexmedetomidine group (group IRD). Cerebral I/R was established by two-vessel occlusion plus hypotension.Dexmedetomidine 25 μg/kg was intraperitoneally injected at 10 min of ischemia in group IRD and at the corresponding time point in group SD.Neurological function was assessed using modified neurological severity score at 1 h of reperfusion.The animals were then sacrificed and brain tissues were taken for determination of the expression of endoplasmic reticulum stress-related proteins such as immunoglobulin heavy chain-binding protein (BIP), eukaryotic translation initiation factor 2α (EIF-2α), phosphorylated EIF-2α (p-EIF-2α), PERK and phosphorylated PERK (p-PERK) (by Wester blot). In the cell experiment, a mouse hippocampal neuronal cell line was selected and divided into 4 groups ( n=12 each) using a random number table method: control group (group C), oxygen-glucose deprivation/restoration (OGD/R) group (group OGD/R), OGD/R+ dexmedetomidine group (group OGD/R+ D) and OGD/R+ ISRIB (PERK pathway inhibitor) group (group OGD/R+ ISRIB). Cells were exposed to 94%N 2-5%CO 2-1%O 2 and incubated in a low-glucose DMEM medium for 6 h followed by restoration to establish OGD/R model.At 30 min before OGD, dexmedetomidine (final concentration 5 mmol/L) was added in group OGD/R+ D, and ISRIB (final concentration 10 mmol/L) was added in group OGD/R+ ISRIB.After 12-h restoration was completed, the cell survival rate was detected by CCK-8 assay.At 24 of restoration, the expression of endoplasmic reticulum stress-related proteins was determined by Wester blot. Results:In the in vivo experiment, compared with group S, neurobehavioral score was significantly increased and the expression of BIP, p-EIF-2α and p-PERK in brain tissues was up-regulated in group IR ( P<0.05). Compared with group IR, neurobehavioral score was significantly decreased and the expression of BIP, p-EIF-2α and p-PERK in brain tissues was down-regulated in group IRD ( P<0.05). In the cell experiment, compared with group C, the expression of BIP, p-EIF-2α, PERK and p-PERK was significantly up-regulated, and the cell survival rate was decreased in group OGD/R ( P<0.05). Compared with group OGD/R, the expression of BIP, p-EIF-2α, PERK and p-PERK was significantly down-regulated, and the cell survival rate was increased in OGD/R+ D, OGD/R+ ISRIB groups ( P<0.05). Compared with group OGD/R+ ISRIB, the expression of PERK was significantly down-regulated ( P<0.05) and no significant change was found in the other parameters in group OGD/R+ D ( P>0.05). Conclusion:The mechanism by which dexmedetomidine reduces cerebral I/R injury may be related to inhibiting PERK pathway-mediated endoplasmic reticulum stress in mice.

Objective : To investigate the effects of dexmedetomidine on inflammatory factors and endoplasmic reticulum stress in myocardial ischemia reperfusion indu~ced brain injury. Methods : Twenty⁃four SPF⁃grade healthy male SD rats , weighing (200 220) g and aged (6 8) weeks , were divided into three groups (n = 8) by random number table method : sham operation group ( S group) myocardial ischemia reperfusion group ( IR group) and myocardial ischemia/reperfusion + Dex group (IR + Dex group) . After the rats were adapted to the feeding environment , the myocardial ischemia reperfusion injury model was established by ligating the anterior descending branch of the left coronary artery for 30 min and reperfusion for 120 min. At the beginning of reperfusion , IR + Dex group was given 25 μg/kg dexmedetomidine , S group and IR group were injected with equal volume normal saline. Rats were sacrificed by decapitation and brain tissue was taken and the changes of hippocampal cell structure of rats stained by HE were observed under light microscope. Serum inflammatory factors IL⁃6 , IL⁃8 and IL⁃10 were detected by ELISA. The expressions of Chop , Bip , p ⁃eif⁃2α and p ⁃perk in rat hippocampal tissues were determined by Western blot. Results : Compared with the S group , the IR group and the IR + Dex group showed aggravation of brain lesions , increased expression of inflammatory cytokines IL⁃6 and IL⁃8 (P < 0. 05) , and decreased expression of IL⁃10 ( P < 0. 05 ) . Hippocampal Chop , Bip , p ⁃eif⁃2α and p ⁃perk proteins were up⁃regulated ( P < 0. 05 ) . Compared with IR group , IR + Dex group showed reduced pathological injury , decreased expression of IL⁃6 and IL⁃8 (P < 0. 05) , increased expression of IL⁃10 (P < 0. 05) , and down⁃regulated expressions of Chop , Bip , p ⁃eif⁃2α and p ⁃perk in hippocampal tissues ( P < 0. 05 ) . Conclusion Dexmedetomidine preconditioning can reduce the brain injury caused by myocardial ischemia reperfusion , and its mechanism may be related to the inhibition of systemic inflammatory response and endoplasmic reticulum stress.