Xuefu Zhuyu decoction (XFZYD) is a famous traditional Chinese medicine (TCM) formula, is widely used in the treatment of cardiovascular and cerebrovascular diseases in China over one hundred years. But its effect on antioxidant and drug-metabolizing enzymes are unknown. This study was to observe the effects of Xuefu Zhuyu decoction (XFZYD) on the activities of antioxidant and drug metabolism enzymes (DMEs) in liver of rats. Male SD rats, treated with XFZYD at the dosage of 3.51, 7.02 and 14.04 g x kg(-1) per day for 15 days, serum were collected, tissue fluid, cytosols and microsomes isolated from liver tissues were prepared by centrifugation according to the standard procedure, the activities of antioxidant enzymes and drug-Metabolizing Enzymes were determined by UV-V is spectrophotometer. In serum, the activities of AST was not significantly affected by the treatment with XFZYD, at the high- est dose, the levels of ALT, Cr and BUN were significantly decreased (P < 0.05). GPX were significantly increased at the dose of 7.02, 14.04 g x kg(-1) (P < 0.05), CAT were significantly increased at the highest dose (P < 0.05). T-SOD was not significantly af- fected by this treatment. In the liver tissue, GPX was significantly increased at the dose of 3.51, 7.02 g x kg(-1) (P < 0.05), GST, CAT and T-SOD were not significantly affected following this treatment. In cytosols, GST was significantly increased at the dose of 3.51 g x kg(-1) (P < 0.05), T-SOD was remarkable induced at the dose of 3.51 and 7.02 g x kg(-1) (P < 0.05). In microsomes, XFZYD had no significant effect on Cytochromeb5, NADPH-Cytochrome P450 reductase, CYP3A, CYP2E1 and UGT, XFZYD significantly in- duced GST at the dose of 3.51 and 7.02 g x kg(-1) (P < 0.05), and the level of GSH were significantly increased by XFZYD at the dose of 3.51, 7.02 and 14.04 g kg(-1) (P < 0.05). These findings suggest XFZYD can induce the activities of GPX, CAT, SOD, GST and increase GSH level in liver of rats, which indicate XFZYD may have detoxification and antioxidant functions.
Animals ; Antioxidants ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Inactivation, Metabolic ; drug effects ; Liver ; drug effects ; enzymology ; Male ; Rats ; Rats, Sprague-Dawley

Objective To analyze the karyotypes of 11 cases of Turner syndrome with marker chromosome,and study the phenotypic effects resulting from the abnormal karyotype.Methods Eleven Turner syndrome patients had a mosaic karyotype and carried a marker chromosome,and 6 marker chromosomes were ring chromosomes.Their karyotypes were showed as mos.45,X/46,X,+mar or mos. 45,X/46,X,+r.Fluorescence in situ hybridization(FISH)technique with X/Y centromere probes was performed to determine the origin of the marker chromosome.Reverse chromosome painting technique was used to identify the breakpoints of two largest markers.Phenotype effects with different chromosome breakpoints were compared.Results All the 11 marker chromosomes were ring X chromosomes.The breakpoints of the r(X)were involved in Xp22,Xq22,Xq24 and Xq26,etc.Conclusions The marker chromosomes in Turner syndrome mainly originate from X chromosome and form ring chromosome X.Each r (X)in our patients was mosaic,indicating it was originated from mitosis error during early embryo development.To analyze the origin of the marker chromosome and the breakpoint of r(X)will provide guidance for the therapy and prognosis of the Turner syndrome patient.

Adult ; Blast Injuries ; therapy ; Explosions ; Humans ; Male ; Multiple Trauma ; therapy

Animals ; Humans ; Oligonucleotide Array Sequence Analysis ; Pharmacogenetics ; trends ; Polymorphism, Genetic

OBJECTIVETo investigate the effects of RNA interference (RNAi) targeting angiotensin II Type 1 receptor (ATlR) and angiotensin-converting enzyme (ACE) on blood pressure and myocardial remodeling in spontaneous hypertensive rats (SHRs).

METHODSSaline (control), adenovirus (Ad5) and recombinant adenoviral vectors (Ad5-ACE-shRNA, Ad5-AT1R-shRNA and Ad5-ACE-AT1R-shRNA expressing ACE, AT1R, ACE and AT1R gene-specific shRNA, respectively) were randomly administered by caudal intravasation to SHRs (n = 12 each group) at day 1 and 17. Normotensive Wistar-Kyoto rats (WKY) served as normal controls. Systolic blood pressure (SBP) of the caudal artery was measured daily. Expression of ACE and AT1R at mRNA levels in ventricle and aorta were evaluated by fluorescence quantitative PCR. Angiotension II serum concentration was measured by ELISA at day 3 (n = 6 each group). The ratio of left ventricular to body weight (LVW/BW) and myocardial collagen content were measured, myocardial ultrastructure observed under transmission electron microscope at the study end.

RESULTSThe caudal artery pressure of saline and Ad5 group was equally increased by about 26 mm Hg(1 mm Hg = 0.133 kPa) compared to baseline (both P < 0.05). Ad5-ACE-shRNA, Ad5-AT1R-shRNA and Ad5-ACE-AT1R-shRNA injection significantly reduced SBP (-24 mm Hg, -22 mm Hg and -26 mm Hg respectively, all P < 0.05 vs. baseline) and the antihypertensive effect could last at least 15 days post each injection. SBP was not affected by saline and Ad5 injections. ACE and AT1 mRNA expressions at ventricle and aorta were significantly decreased in Ad5-ACE-shRNA, Ad5-ACE-AT1R-shRNA and Ad5-AT1R-shRNA, Ad5-ACE-AT1R-shRNA treated SHRs compared to those in saline and Ad5 groups (all P < 0.05) and was comparable to that in WKY group (P > 0.05). The LVW/BW ratio [(2.22 +/- 0.18) microg/mg, (2.23 +/- 0.19) microg/mg, (2.17 +/- 0.16) microg/mg] and myocardial collagen content [(1.291 +/- 0.019) microg/mg, (1.298 +/- 0.019) microg/mg, (1.276 +/- 0.019) microg/mg] in Ad5-ACE-shRNA, Ad5-AT1R-shRNA and Ad5-ACE-AT1R-shRNA treated SHRs were also significantly lower than those in saline treated [(3.23 +/- 0.13) microg/mg and(1.683 +/- 0.013) microg/mg, both P < 0.05] and Ad5 treated SHRs [(3.25 +/- 0.12) microg/mg and(1.693 +/- 0.013) microg/mg, both P < 0.05], but still higher than those of WKY group [(2.06 +/- 0.12) microg/mg and (1.258 +/- 0.019) microg/mg, both P < 0.05]. Myocardial ultrastructure was also significantly improved in all SHRs underwent RNAi treatments compared to saline and Ad5 treated SHRs.

CONCLUSIONRNAi targeting ACE and AT1R gene significantly inhibited myocardial and aortic ACE and AT1R mRNA expressions and resulted in prolonged antihypertensive effects and myocardial ultrastructure improvements in SHRsl. The RNAi technology may be a potential new strategy of gene therapy for hypertension.

Animals ; Blood Pressure ; Gene Silencing ; Heart Rate ; Hypertension ; genetics ; physiopathology ; Male ; Peptidyl-Dipeptidase A ; genetics ; metabolism ; RNA Interference ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptor, Angiotensin, Type 1 ; genetics ; metabolism ; Ventricular Remodeling

The paper is to report the development of a high-performance liquid chromatographic/tandem mass spectrometry (HPLC-MS/MS) method for the determination of icaritin (ICT) in rat plasma. After precipitated with acetonitrile from the plasma, ICT was isolated chromatographically on a Dikma C18 column. The mobile phase consisted of acetonitrile-water-acetic acid (72 : 28 : 1.5, v/v/v). Electrospray ionization (ESI) source was applied and operated in the positive ion mode. Multiple reaction monitoring (MRM) mode with the transitions of m/z 387 --> m/z 313 and m/z 331 --> m/z 315 were used to quantify ICT and the internal standard, respectively. The linear calibration curve was obtained in the concentration range of 2.5-1,000 ng x mL(-1). The lower limit of quantification was 2.5 ng x mL(-1). The inter- and intra-day precision (RSD) were less than 9.63%, and the accuracy (relative error) was within +/-7.42%. The method was proved to be suitable for the pharmacokinetics of ICT, which offers advantages of high sensitivity and selectivity.
Administration, Oral ; Animals ; Chromatography, High Pressure Liquid ; methods ; Epimedium ; chemistry ; Female ; Flavonoids ; administration & dosage ; blood ; isolation & purification ; pharmacokinetics ; Male ; Plants, Medicinal ; chemistry ; Rats ; Rats, Wistar ; Reproducibility of Results ; Sensitivity and Specificity ; Spectrometry, Mass, Electrospray Ionization ; methods ; Tandem Mass Spectrometry ; methods

OBJECTIVETo investigate the combined effects between the two polymorphisms murine double minute 2 (MDM2) rs2279744 T→G and P53 rs1042522 G→C on the genetic susceptibility of breast cancer.

METHODSA total of 600 female patients with diagnosed breast cancer were consecutively recruited from the Yuhang district, Hangzhou city during March 2001 to May 2009. In the same period as the cases were collected, 600 healthy women living in Yuhang district, Hangzhou city were selected from a nutritional survey conducted. Peripheral blood lymphocytes were obtained from the study subjects and the demographic information were collected through questionnaires. PCR-restriction fragment length polymorphism (PCR-RFLP) was used for genotyping MDM2 rs2279744 T→G and P53 rs1042522 G→C. Logistic regression analysis was used to analyze the combined effects of the two polymorphisms on breast cancer risk.

RESULTSThe frequency of MDM2 rs2279744 GG, TG and TT genotypes were 31.5% (189/600), 45.5% (273/600), 23.0% (138/600) in case group and 19.0% (114/600), 49.2% (295/600), 31.8% (191/600) in control group. The frequency of P53 rs1042522 GG, GC and CC genotypes were 23.1% (139/600), 50.2% (301/600), 26.7% (160/600) in case group and 30.5% (183/600), 51.3% (308/600), 18.2% (109/600) in control group. Logistic regression analysis showed that carriers with rs2279744 TG, GG genotypes had a significant increased risk for developing breast cancer compared with rs2279744 TT carriers (OR = 1.31, 95%CI: 0.97 - 1.73 for TG; OR = 2.24, 95%CI: 1.61 - 3.09 for GG). When comparing with rs1042522 GG carriers, carriers with rs1042522 GC, CC genotypes had a significant increased risk for developing breast cancer (OR = 1.34, 95%CI: 0.94 - 1.68 for GC; OR = 1.89, 95%CI: 1.35 - 2.68 for CC). The united analysis of this two polymorphisms showed that compared with individuals carrying rs2279744 TT and rs1042522 GG (the frequency were 4.8% (29/600) in case group and 11.5% (69/600) in control group), carries with rs2279744 TG/GG and rs1042522 GC/GG genotypes (the frequency were 95.2% (571/600) in case group and 88.5% (531/600) in control group) showed significant higher risk in the susceptibility to breast cancer (OR = 2.30, 95%CI: 1.39 - 3.82 for TG/GC + GG; OR = 2.14, 95%CI: 1.29 - 3.55 for TT + GC/CC; OR = 2.86, 95%CI: 1.80 - 4.53 for TG/GG + GC/CC). The combination of MDM2 rs2279744 T→G and P53 rs1042522 G→C contributed to a significantly higher risk of breast cancer than did any one of the variant (P = 0.046). The risk of susceptibility to breast cancer was much higher when this two polymorphisms both variant.

CONCLUSIONSThe MDM2 rs2279744 T→G and P53 rs1042522 G→C may be risk factor for breast cancer. Significant combined effects between the two polymorphisms may contribute to the genetic susceptibility to breast cancer.

Adult ; Breast Neoplasms ; genetics ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Middle Aged ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-mdm2 ; genetics ; Risk Factors ; Tumor Suppressor Protein p53 ; genetics

OBJECTIVETo test the association between XRCC1 gene polymorphisms and susceptibility of nasopharyngeal carcinoma in Cantonese nuclear families through a family-based association study.

METHODSA total of 2134 study subjects from 457 Cantonese nuclear families were recruited in the study. Each family had two parents and at least one offspring with nasopharyngeal carcinoma. Genotyping for three single nucleotide polymorphisms in XRCC1 gene, including rs1799782 (C > T), rs25489 (G > A) and rs25487 (G > A), were performed with PCR-RFLP assay. The genotype data were analyzed with family-based association test (FBAT) software to check linkage and association between the three genetic markers and susceptibility of nasopharyngeal carcinoma.

RESULTSFBAT analysis showed XRCC1 gene genotypes and haplotypes were not significantly associated with nasopharyngeal carcinoma in our study population (rs1799782: chi(2) = 1.006, P = 0.605; rs25489: chi(2) = 0.470, P = 0.790; rs25487: chi(2) = 2.563, P = 0.278; haplotype: chi(2) = 3.004, P = 0.557, global statistic). For rs25487, the G allele (major allele) showed increased transmission under dominant model (Z = 1.985, P = 0.047). Whereas the C allele (minor allele) exhibited reduced transmission under recessive model (Z = -1.985, P = 0.047). However, no increased/reduced transmission was observed under additive model and with global statistic.

CONCLUSIONThere is no evidence of an association between polymorphisms in XRCC1 gene and susceptibility of nasopharyngeal carcinoma in Cantonese nuclear families is observed in this study.

DNA Damage ; DNA Repair ; DNA-Binding Proteins ; genetics ; Gene Frequency ; Genotype ; Humans ; Nasopharyngeal Neoplasms ; genetics ; Pedigree ; Polymorphism, Single Nucleotide ; Surveys and Questionnaires ; X-ray Repair Cross Complementing Protein 1

OBJECTIVETo uncover the transmission patterns of the HIV epidemic in Dehong prefecture.

METHODSThe reviewed case reports, data of sentinel surveillance, testing and special survey were analyzed by SAS 8.0 program. The transmission patterns were modeled by utilizing data including sizes of the whole population and the high risk groups, high risk behavior data from 1989 to 2007, and the population index such as sex ratio and fertility rate.

RESULTSIn 2005, case reports showed the proportion of people infected with HIV through sexual contact was 39.1%, and 46.9% in 2006. Among 1636 cases reported between January 1 to September 20, 2007, the proportion of people infected with HIV through sexual contact was 52%. From 1989 to 2007, the proportion of HIV infection among drug users was declining, while HIV infection through sexual contact was rising after standardizing the population tested/surveyed. The Asian Epidemic Model has shown that the proportions of incident HIV infections through sexual transmissions were 50.6%, 52.3% and 52.7% respectively from 2005 to 2007. Correspondingly, the proportions of incident cases by injecting drug user were 48.9%, 47.2% and 46.7% respectively during this period. Moreover, the Workbook method has shown that, among adults living with HIV in 2007, 50.3% were infected through injecting drugs and 48.4% through unsafe sexual activity.

CONCLUSIONThe rapid rise in HIV infections through injecting drug in Dehong prefecture has been initially curbed. HIV epidemic has already witnessed a change from predominantly through drug injecting-related activity to an almost equally fuelled epidemic by sexual and drug-related transmission.

Acquired Immunodeficiency Syndrome ; epidemiology ; transmission ; China ; epidemiology ; Humans ; Models, Statistical ; Risk Factors ; Social Problems

OBJECTIVETo determine the karyotype of a patient with Prader-Willi-like syndrome features.

METHODSChromosomal high resolution banding was carried out to analyze the karyotype of the patient, and methylation-specific PCR was used to analyze the imprinting region of chromosome 15. Subtelomeric region was screened by multiplex ligation-dependent probe amplification (MLPA), and fluorescent in situ hybridization (FISH) and real-time quantitative PCR were further performed to identify the deleted region.

RESULTSNo abnormality was discovered by high resolution karyotype analysis and methylation-specific PCR studies. MLPA analysis showed that the patient had a deletion of 1p subtelomeric area, which was confirmed by FISH analysis. The deleted region was shown within a 4.2 Mb in the distal 1p by 3 BAC FISH probes of 1p36 combined with real-time PCR technique. Family pedigree investigation showed the chromosome abnormality was de novo. Therefore, partial monosomy 1p36 was likely responsible for the mental retardation of the patient.

CONCLUSIONMolecular cytogenetic techniques should be performed to those patients with Prader-Willi-like syndrome features, to determine their karyotypes.

Child ; Chromosome Deletion ; Chromosomes, Human, Pair 1 ; genetics ; Female ; Humans ; Karyotyping ; Prader-Willi Syndrome ; genetics