Objective To screen the optimized Buyang Huanwu Decoction (BYHWD);To verify it. Methods H2O2 was used to induce PC12 cell oxidative stress models. MTT method was used to determine the prevention effects of BYHWD at different concentrations (0.1, 0.2, 0.5, 1.0, 2.0, 3.5 mg/mL) on in vitro oxidative stress cell models to define the optimized concentration. Orthogonal design was used to divide BYHWD single medicine into decomposed BYHWD groups, control group (only with DMEM), normal group (without H2O2 and medicine processing), and model group, to investigate the protective effects on PC12 cells. Optimized BYHWD was screened to decide the compatibility ratio of each medicine. MTT was used to detect the cell survival rate in each group. Middle cerebral artery occlusion was used to replicate MACO rat models. SD rats were randomly divided into sham-operation group, model group, BYHWD group and optimized BYHWD high-, medium-and low-dose groups. Each medication group was given relevant medicine for gavage. The screened results were verified. Results Compared with other decomposed BYHWD groups, the protective effects of the compatibility of Astragali Radix+Chuanxiong Rhizoma+Pheretima on PC12 cells was the best (P<0.05), which was nearly equaled to BYHWD. Compared with the model group, BYHWD and the optimized one could evidently reduce cerebral cortex infarction area and improve the impaired brain edema (P<0.05), and the medium-dose group was the best. Conclusion The optimized BYHWD ratio is:Astragali Radix:Chuanxiong Rhizoma:Pheretima=10:3:1.

The purpose of this study is to assess the effects of anti-inflammatory on activation of nuclear factor-kappaB and mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in intestinal mucosal biopsy specimens from patients with ulcerative colitis (UC). A total of 27 cases with UC were investigated. 15 cases received sulfasalazine (SASP) treatment or SASP and glucocorticoid treatment, 12 cases did not receive any medication related with UC. Normal mucosa from 9 colon cancer cases served as control. Ten pieces of intestinal mucosal biopsy specimens were obtained from each patient. The mRNA expression of ICAM-1 and VCAM-1 were determined by reversal transcription-polymerase chain reaction (RT-PCR). The protein levels of ICAM-1 and VCAM-1 were measured by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay (EMSA). The results showed that NF-kappaB DNA binding activity, mRNA and protein expression of ICAM-1 and VCAM-1 were increased significantly in patients with UC, compared with normal control (P<0.05). Glucocorticoids and SASP markedly inhibited NF-kappaB activation and significantly decreased mRNA and protein expression of ICAM-1 and VCAM-1 (P<0.05). Adhesion molecules (ICAM-1 and VCAM-1) gene activation had significant positive correlation with the NF-kappaB DNA binding activity (r=0.8652 P<0.05, r=0.7902, P<0.05, respectively). We concluded that NF-kappaB is a major and essential factor in regulating the expression of adhesion molecules, it plays an important role in the pathogenesis of UC. SASP and glucocorticoids ameliorate UC via inhibition of NF-kappaB activation and reduction of adhesion molecules expression.
Adult ; Anti-Inflammatory Agents ; therapeutic use ; Colitis, Ulcerative ; drug therapy ; metabolism ; Female ; Humans ; Intercellular Adhesion Molecule-1 ; biosynthesis ; genetics ; Intestinal Mucosa ; metabolism ; Male ; NF-kappa B ; metabolism ; Prednisone ; therapeutic use ; RNA, Messenger ; biosynthesis ; genetics ; Sulfasalazine ; therapeutic use ; Vascular Cell Adhesion Molecule-1 ; biosynthesis ; genetics

OBJECTIVE: To evaluate the accuracy of cerebral state index (CSI) as an indicator of anesthesia depth in patients in the induction of anesthesia with target-controlled infusion of propofol. METHODS: Forty ASA (American Society of Anesthesiologists) I approximately II patients scheduled for an operation under general anesthesia were anesthetized with target-controlled infusion of propofol. Target plasma concentration was 0. 5 mg/L at the beginning, and increased by 0. 5 mg/L every 5 minutes, till 5 minutes after the level of MOAA/S (modified observer's assessment of alertness/sedation) was 0. The CSI, mean arterial pressure (MAP), heart rate (HR), MOAA/S level, and the effect-site concentration of propofol were recorded. RESULTS: (1) CSI values declined with the decrease of MOAA/S levels. CSI values were statistically different between level 0 and 1, level 1 and 2, level 3 and 4, level 4 and 5 of MOAA/S (P < 0.05). The difference of MAP had statistical significance between level 3 and level 2 of MOAA/S (P < 0.05). HR values had no statistical difference between the two levels of MOAA/S (P > 0.05). (2) The spearman rank correlation co-efficients between CSI, MAP, HR and the level of MOAA/S were 0.929, 0.421, and 0.085, respectively. The prediction probabilities (Pk) to differentiate different levels of MOAA/S for CSI, MAP, and HR were 0.94, 0.67, and 0.54, respectively. (3) There was linear regression relationship between CSI and the effect-site concentration of propofol (the coefficient of determination R2 was 0. 833, P < 0.01). CONCLUSION During the induction of patients with target-controlled infusion of propofol, the CSI is accurate as an indicator of awakeness and different levels of consciousness after anesthesia, and can reliably predict the anesthesia depth.
Adjuvants, Anesthesia ; Adult ; Anesthesia, General ; Anesthetics, Intravenous ; Cerebral Cortex ; drug effects ; physiology ; Female ; Humans ; Male ; Monitoring, Intraoperative ; methods ; Propofol

Objective To investigate and analyze the related factors influencing the quality of life in patients with epilepsy, and provide a theoretical basis for taking appropriate measures to improve the quality of life in patients with epilepsy. Methods Sixty-five patients with epilepsy visiting our hospital from July 2007 to December 2008 were chosen in our study. The table-31 for quality of life in patients with epilepsy (Chinese version) was performed on them. The age, gender, education degree,seizure types, course of disease, cognitive function, medication compliance and fear of attack were considered as the independent variable; related factors in the table-31 for quality of life were adopted as dependent variable; multiple linear regression analysis was performed on these 2 variables. Results Education degree and course of disease could affect the memory of patients with epilepsy (standardized regression coefficients were 0.380 and 0.264, respectively). Age could affect the social activities of the patients (standardized regression coefficient was -0.303). Gender could affect the attack of the patients (standardized regression coefficient was 0.332). Conclusion The influencing factors of quality of life in patients with epilepsy are age, gender, education degree, course of disease; and education degree and course of disease enjoy the greatest influence.

Clinical epidemiologic data and animal experimental studies regard estrogen as being protective against the development of cardiovascular diseases. The mechanisms by which estrogen affects the development of vascular diseases are not clear. Recent studies demonstrated that the cardiovascular protective effects of estrogen are closely related to nitric oxide (NO) pathway. Our previous study proved that estrogen inhibited the proliferation and oncogene expression of vascular smooth muscle cells (VSMCs) induced by endothlin 1 (ET-1) and serum,this effect was mediated by NO release. In the present study, we investigated the role of inducible nitric oxide synthase (iNOS) in the VSMCs cycle arrest induced by 17 beta-estradiol (E(2)). The effects of E(2) on iNOS activity and protein expression in cultured rat VSMCs and the influence of NOS inhibitor N(G)-nitro-L-arginine methylester (L-NAME) on the inhibitory effect of E(2) on cell cycle were investigated. NOS assay kit was used to measure the activity of iNOS and protein expression of iNOS was determined by Western-blot. Cell cycle analysis was accessed by flow cytometry. The results obtained showed that E(2) increased iNOS activity of VSMCs but not in a dose-dependent manner. E(2) 10 nmol/L increased the iNOS activity of VSMCs distinctly at two time points: 30 min and 12 h. These effects were significantly inhibited by estrogen receptor (ER) antagonist Tamoxifen (0.1 micromol/L) and NOS inhibitor L-NAME (1 micromol/L). E(2) increased iNOS protein expression of VSMCs in a dose-dependent manner. The effect of E(2) on iNOS protein expression of VSMCs started at 3 h, distinctly increased at 12 h and then decreased. Tamoxifen significantly inhibited the E(2)-induced iNOS protein expression of VSMCs. ET-1 increased cell percentage of S phase and G(2)+S/G(1). This effect was inhibited by E(2). L-NAME significantly attenuated the inhibitory effect of E(2) on cell cycle of VSMCs. The results suggest that E(2) induced G(1) arrest of VSMCs, which was associated with an increase in iNOS activity and protein expression of VSMCs. These effects were at least mediated by estrogen receptor partly.
Animals ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Cells, Cultured ; Endothelin-1 ; metabolism ; Estradiol ; pharmacology ; Estrogen Antagonists ; pharmacology ; Female ; Muscle, Smooth, Vascular ; cytology ; Nitric Oxide Synthase ; metabolism ; physiology ; Nitric Oxide Synthase Type II ; Rats ; Tamoxifen ; pharmacology

Rat vascular smooth muscle cells (VSMC) were used to study the effect of 17beta -estradiol (E(2)) on cellular proliferation (cell counting), DNA synthesis ((3)H thymidine incorporation), MTT, c -fos mRNA expression and nitric oxide (NO) release. The results obtained showed that E(2) (10(-12) 10(-8) mol/L) induced NO release from VSMC in a concentration-dependent manner; 10(-8) mol/L E (2)significantly inhibited VSMC cellular proliferation and DNA synthesis induced by 10% FCS and 10(-7) mol/L ET-1, which was obviously reversed by 10(-7)mol/L tamoxifen and 10(-6) mol/L L-NAME; after a pretreatment for 24 hours, 10(-8)mol/L E(2) significantly inhibited VSMC c -fos mRNA expression induced by 10(-7)mol/L ET-1, which was also obviously reversed by 10(-6) mol/L L-NAME. These results suggest that the inhibitory effects of E(2) on VSMC cellular proliferation and c -fos mRNA expression are closely related with NO release in VSMC, which is, at least, partly medicated by ER.
Animals ; Cell Division ; drug effects ; Cells, Cultured ; Estradiol ; pharmacology ; Female ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Nitric Oxide ; metabolism ; physiology ; Proto-Oncogene Proteins c-fos ; biosynthesis ; RNA, Messenger ; biosynthesis ; Rats ; Rats, Sprague-Dawley

Advanced technologies are used to clarify the meridian tropism theory of traditional Chinese medicine is an important part of theoretical studies of traditional Chinese medicine. In this article, modern pharmacokinetic method was used to investigate tissue distribution characteristics of psoralen and isopsoralen of Psoraleae Fructus decoction in rats, in order to provide research ideas and experimental basis for the meridian tropism theory. In this study, various tissue samples such as heart, liver, spleen, lung, kidney, brain and spermary were collected at different times after oral administration with FP decoction, in order to determine concentration of psoralen and isopsoralen by HPLC. Pharmacokinetic parameters were calculated by DAS 2.0 software. The study results showed that HPLC indexes of psoralen and isopsoralen in various tissues of rats met the determination requirements of biological samples. Both components were distributed in all of the tissues, with AUC(0-t) order of liver > lung approximately kidney > heart > brain approximately spleen > spermary. There was significant difference between liver, kidney, lung and other tissues (P < 0.05). MRT(0-t) of both psoralen and isopsoralen were about 10 h. Therefore, psoralen and isopsoralen showed stronger targeting selection in liver, kidney and lung.
Animals ; Area Under Curve ; Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; administration & dosage ; pharmacokinetics ; Fruit ; chemistry ; Furocoumarins ; pharmacokinetics ; Kinetics ; Male ; Plant Extracts ; administration & dosage ; chemistry ; pharmacokinetics ; Psoralea ; chemistry ; Rats ; Tissue Distribution

In the present study, confluent bovine aortic endothelial cells (BAECs) were used to study the rapid nongenomic effects of 17beta-estradiol and the membrane impermeable conjugated 17beta-estradiol (E(2)BSA) on the activation of endothelial nitric oxide synthase (eNOS) and mitogen activated protein kinase (MAPK). eNOS activation was assessed in whole cells by measuring [(3)H]L-arginine conversion to [(3)H]L-citrulline. MAPK activity was determined by Western blotting. The results obtained show that the addition of various concentrations of E(2) (0.001-1 micromol/L) resulted in 122+/-29, 186+/-17, 83+/-20 and 157+/-29% increases in eNOS activity, respectively, in BAECs within 15 min of exposure to the hormone. E(2) (0.01 mol/L)-stimulated eNOS activity was detectable during 5-, 15- and 30- min incubation which yielded increases of 37+/-6, 56+/-9 and 38+/-8%, respectively. The increase reached a plateau from 15 through 30 min and rapidly declined thereafter. E(2)BSA 17.5 ng/ml also enhanced eNOS activity by an increase of 35+/-9% above the basal activity. The effect of E(2) and E(2)BSA on eNOS activation was unaffected by actinomycin D 25 microg/ml but was obviously inhibited by tamoxifen (0.1 micromol/L) and PD98059 (50 micromol/L). Compared with control E(2) and E(2)BSA stimulation of BAECs for 15 min caused an increase in MAPK activity by 428+/-17 and 360+/-14% respectively. This effect was blocked by tamoxifen. These results suggest that there might be the membrane estrogen receptor localized on BAECs, which mediates the rapid nongenomic effect of estrogen on eNOS activation through MAPK pathways.
Animals ; Aorta ; cytology ; Cattle ; Cell Membrane ; metabolism ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Estradiol ; pharmacology ; Mitogen-Activated Protein Kinases ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Receptors, Estrogen ; physiology

OBJECTIVE: To examine the predicted effect-site concentration of propofol at two clinical end-points: loss of verbal contact (LVC) and loss of consciousness (LOC), and to explore the relationship between bispectral index (BIS) values, cerebral state index (CSI) values and the predicted effect-site concentration during the target-controlled infusion of propofol. METHODS: In 20 patients during the target-controlled infusion of propofol, the propofol infusion was set at an initial effect-site concentration of 0.5 mg/L, and increased by 0.5 mg/L every 5 min until 5 min after the modified observer's assessment of alertness/sedation scale (OAA/S) values reached zero. The predicted effect-site concentration of propofol, the values of CSI and BIS were recorded, and the sedation level was examined by the modified OAA/S every 20s. The predicted effect-site concentrations of propofol in target-controlled infusion (TCI) system were recorded when they increased by more than 0.1 mg/L. The predicted effect-site concentrations of propofol and the values of BIS and CSI at LVC and LOC in 5%, 50% and 95% of the patients were calculated. RESULTS: There was good linearity between BIS and the predicted effect-site concentration of propofol (R(2)=0.787), as well as between CSI and the predicted effect-site concentration of propofol (R(2)=0.792). The predicted effect-site concentrations of propofol at LVC in 5%, 50% and 95% of the patients were 1.1,1.8 and 2.4 mg/L, respectively. The values of BIS and CSI at LVC in 5%, 50% and 95% of the patients were 79.2, 69.2 and 59.2; 74.9, 65.9 and 56.8, respectively. The predicted effect-site concentrations of propofol at LOC in 5%, 50% and 95% of the patients were 1.5, 2.5 and 3.4 mg/L, respectively. At LOC, the values of BIS and CSI in 5%, 50% and 95% of the patient were 73.6, 57.1 and 40.6; 65.2, 54.8 and 44.3, respectively. CONCLUSION During target-controlled infusion of propofol, LVC and LOC occur within a definite range of predicted effect-site concentrations. There is the good linearity between BIS, CSI and the predicted effect-site concentrations of propofol. CSI may be more useful than BIS in predicting LVC and LOC.
Adult ; Anesthetics, Intravenous ; administration & dosage ; pharmacology ; Electroencephalography ; Female ; Humans ; Male ; Monitoring, Intraoperative ; Propofol ; administration & dosage ; pharmacology

The morbidity and mortality of cardiovascular diseases are very high, which has attracted more and more attention all over the world. Common treatment methods for clinical treatment of acute myocardial infarction include direct percutaneous coronary intervention and coronary artery bypass grafting, which can quickly restore blocked coronary blood flow and reduce the infarct size. However, the inevitable ischemia/reperfusion injury will occur during the recovery of coronary blood flow, its pathological mechanism is complicated, and the Western medicine countermeasures are very limited. Among the current drugs for the treatment of cardiovascular diseases, traditional Chinese medicine has become a research hotspot due to its multiple targets, safety, and low side effects. Ginger is the fresh rhizome of Zingiber offici?nale Rosc., a perennial herbaceous plant in the ginger family. It is a dual-purpose resource of medicine and food. Ginger has the functions of relieving the appearance and dispelling cold, warming up and relieving vomiting, resolving phlegm and relieving cough, and relieving fish and crab poison. The chemical components of ginger mainly include volatile oil, gingerol, diphenylheptane, etc.. Among them, 6-gingerol, as the main active component of gingerols, has obvious phar?macological effects in myocardial protection, anti-oxidation, anti-inflammatory, etc.. Studies have shown that 6-gingerol protects myocardium mainly through anti-oxidative stress, anti-inflammatory, inhibiting cell apoptosis, and preventing cal?cium influx. ① Anti-oxidative stress: oxidative stress is a state where oxidation and anti-oxidation in the body are out of balance, and it is also an important factor leading to myocardial damage. Many studies have confirmed that 6-gingerol has an antioxidant effect, and it is considered a natural antioxidant. 6-gingerol can significantly reduce the degree of oxi?dative stress and the level of reactive oxygen species caused by cardiomyocyte damage, and has a significant cardiopro?tective effect. ② Anti-inflammatory: inflammation can cause substantial cell damage and organ dysfunction, which is another important cause of myocardial damage. 6-gingerol can reduce the levels of inflammatory factors such as inter?leukin-6, interleukin-1β, and tumor necrosis factor-αin cardiomyocytes, and at the same time inhibit the TLR4/NF-κB sig?naling pathway, an important regulatory pathway of inflammation, showing that it may improve myocardial damage through anti-inflammatory effects. ③ Inhibition of apoptosis: apoptosis is a complex and orderly process in the autono?mous biochemical process of cells, and one of the main mechanisms of myocardial injury. This process can be roughly divided into three pathways: mitochondria, endoplasmic reticulum, and death receptors. Among them, the mitochondrial pathway plays an important role, and Bcl-2 and Bax located upstream of this pathway can regulate the entire process of cell apoptosis by regulating the permeability of the mitochondrial membrane. Studies have found that the preventive application of 6-gingerol can reduce cell damage, reduce the number of apoptotic cells, reduce the activity of Bax and caspase-3, and increase the expression of Bcl-2. Therefore, 6-gingerol pretreatment can reduce the damage of cardio?myocytes, and its mechanism may be related to the inhibition of apoptosis.④Prevent calcium influx:calcium overload is involved in the pathogenesis of myocardial ischemic injury, which may be related to excessive contracture, arrhythmia, and mitochondrial Ca2+accumulation that impairs myocardial function. 6-gingerol inhibits the increase of intracellular Ca2+concentration by inhibiting L-type calcium current, thereby reducing extracellular Ca2+ influx, thereby avoiding calcium overload and playing a cardioprotective effect. In summary, 6-gingerol can effectively treat and improve myocardial isch?emia/reperfusion injury, and it has great development potential in the fields of medicine and health products.