Puerarin enhances superoxide dismutase activity and inhibits RAGE and VEGF expression in retinas of STZ-induced early diabetic rats

Objective:To investigate the effects of puerarin on the activity of superoxide dismutase(SOD), and expressions of advanced glycation end-product(AGE) receptor(RAGE) and vascular endothelial growth factor(VEGF) in retinas of streptozotocin(STZ)-induced early diabetic rats. Methods:Diabetic rat models were established by inducing diabetes via intra-peritoneal injection of STZ.Rats were randomly divided into normal(control),diabetic(DM),and DM+ puerarin groups.After intra-gastric administration of puerarin(500 mg/kg/day for 4 weeks),levels of SOD and malondialdehyde(MDA) were determined in serum and retina.mRNA and protein expression levels of RAGE and VEGF in retinas were determined by real-lime polymerase chain reaction(RT-PCR)(mRNA) and Western blot analysis(protein levels).Results:There was significantly lower SOD activity and significantly higher MDA in serum and retinas of the DM group compared with the two other groups(P【0.05).After treatment with puerarin,SOD activity increased and MDA content decreased in this group(P【0.05).mRNA and protein expression levels of RACE and VECF in the DM group were significantly higher than those of the other groups (P【0.05),and decreased after puerarin treatment(P【0.05).Conclusions:Puerarin is able to enhance SOD activity,and inhibit RAGE and VEGF expressions in retinas of STZ-induced early diabetic ruts.

Detection of RASSF1A promoter hypermethylation in serum from gastric and colorectal adenocarcinoma patients

AIM：To evaluate the diagnostic role of serum RASSF1A promoter hypermethylation in gastric and colorectal adenocarcinoma. METHODS：Methylation-specific polymerase chain reaction （MSPCR） was used to examine the promoter methylation status of the serum RASSF1A gene in 47 gastric adenocarcinoma patients, 45 colorectal adenocarcinoma patients, 60 patients with benign gastrointestinal disease （30 with benign gastric disease and 30 with benign colorectal disease）, and 30 healthy donor controls. Apaired study of RASSF1A promoter methylation status in primary tumor, adjacent normal tissue, and postopertive serum were conducted in 25 gastric and colorectal adenocarcinoma patients who later were underwent surgical therapy. RESULTS：The frequencies of detection of serum RASSF1A promoter hypermethylation in gastric （34.0%） and colorectal （28.9%） adenocarcinoma patients were significantly higher than those in patients with benign gastric （3.3%） or colorectal （6.7%） disease or in healthy donors （0%） （P 〈 0.01）. The methylation status of RASSF1A promoter in serum samples was consistent with that in paired primary tumors, and the MSPCR results for RASSF1A promoter methylation status in paired preoperative samples were consistent with those in postoperative serum samples. The serum RASSF1A promoter hypermethylation did not correlate with patient sex, age, tumor differentiation grade, surgical therapy, or serum carcinoembryonic antigen level. Although the serum RASSF1A promoter hypermethylation frequency tended to be higher in patients with distant metastases, there was no correlation between methylation status and metastasis. CONCLUSION：Aberrant CpG island methylation within the promoter region of RASSF1A is a promising biomarker for gastric and colorectal cancer.

Diagnostic Performance of the GenoType MTBDRplus and MTBDRs/Assays to Identify Tuberculosis Drug Resistance in Eastern China

Background： The WHO recently has recommended the GenoType MTBDRph/s version 1.0 and MTBDRs/version 1.0 assays for widespread use in countries endemic with drug-resistant tuberculosis. Despite this, these assays have rarely been evaluated in China, where the burden of drug-resistant tuberculosis is among the highest globally. Methods： Mycobacterium tuberculosis clinical isolates were obtained between January 2008 and December 2008. Isolates were tested for drug resistance against rifampicin （RFP） and isoniazid （INH） using the GenoType MTBDRplus assay and drug resistance against ethambutol （EMB）, ofloxacin （OFX）, and kanamycin （KM） using the Genotype MTBDILsl assay. These results were compared with conventional drug-susceptibility testing （DST）. Results： Readable results were obtained from 235 strains by GenoType MTBDRphts assay. Compared to DST, the sensitivity of GenoType MTBDRplus assay to detect RFP, INH, and multidrug resistance was 97.7%, 69.9%, and 69.8%, respectively, whereas the specificity for detecting RFP, INH, and multidrug resistance was 66.7%, 69.2%, and 76.8%, respectively. The sensitivity and specificity of the GenoType MTBDRsl assay were 90.9% and 95.2% for OFX, 77.8% and 99.5% for KM, 63.7% and 86.4% for EMB, respectively. Mutations in codon S531L of the rpoB gene and codon S315T1 ofKatG gene were dominated in multidrug-resistant tuberculosis （MDR-TB） strains. Conclusions： In combination with DST, application of the GenoType MTBDRplus and MTBDRsl assays may be a useful supplementary tool to allow a rapid and sale diagnosis of multidrug resistance and extensively drug-resistant tuberculosis.