OBJECTIVE:To establish derivative spectrophotometry for the determination of the main component of Captopril tablets.METHODS:Under the alkaline condition of sodium hydroxide,2,4-dinitrofluorobenzene was used as derivatization reagent to react with captopril at 40 ℃ in the water bath.Then UV spectrophotometry was adopted to detect the content of captopril with detection wavelength set at 342 nm.RESULTS:The linear range of captopril was 1.0～14.0 ?g?mL-1(r=0.999 9) with an average recovery of 99.61%(RSD=1.27%,n=9).The RSD of intra-day and inter-day both were less than 2%.CONCLUSION:This method is stable,reliable,rapid and simple for the determination of the main components of Captopril tablets.

Objective To explore the effect of xanthine oxidase inhibitor allopurinol on cardiomyocyte apoptosis in rats after myocardial infarction(MI).Methods MI model was established by the ligation of anterior descending coronary artery.The survivors were randomly divided into 3 groups: sham operation group(n=5),MI group(n=16) and allopurinol group(n=15,receiving allopurinol 50 mg?kg-1? d-1).After 28 days,the infarct size was measured.In non-infarcted zone(NIZ),cardiomyocyte apoptosis was detected by TUNEL;the expression of Fas was detected by immunohistochemistry;the expressions of xanthine oxidase(XO) and caspase 3 were detected by Western blot.In addition,the activities of XO and ?O-2,?OH-scavenging in NIZ were detected by colorimetry.Results Compared with sham operation group,the apoptosis index and expressions of Fas,XO,caspase 3 in NIZ were significantly increased in MI group.The activity of XO was increased but the activities of ?O-2 and ?OH-scavenging were decreased(P0.05).Conclusion Allopurinol could inhibit the cardiomyocyte apoptosis in NIZ in rats.The protective mechanism of allopurinol involves the reduction of reactive oxygen species and depression of the expressions of Fas and caspase 3.

Objective To explore the effect of xanthine oxidase inhibitors allopurinol on collagen remodeling of non-infarcted myocardium after myocardial infarction in rats.Methods Myocardial infarction models were produced by ligation of anterior descending coronary artery.The survivals were randomly divided into 3 groups:sham operation group, MI group and allopurinol group(50 mg/kg).On the 7th, 14th, 21st and 28th day respectively, the collagen content were examined. The type Ⅰ and type Ⅲ collagen volume fraction(CVF) and Ⅰ/Ⅲ ratio in non-infarcted zones(NIZ) were examined with PSR staining, mRNA expressions were detected with RT-PCR, the activities of xanthine oxidase(XO) and O—?2,?OH-scavenging in NIZ were examined by colorimetry.In addition, the expression of XO protein by Western blotting analysis and pathological change in LV were detected on the 28th day.ResultsCompared with sham group,the mRNA expressions, CVF of typeⅠand type Ⅲ collagen in NIZ were increased in MI group.The typeⅠ/Ⅲ ratio in NIZ was increased after decreased.The collagen content and activity of XO were boosted but the activities of O—?2,?OH-scavenging were decreased(P

Objective: To establish a method for the determination of cinnamic acid in Lingguizhugan Decoction (Poria, Ramuls Cinnamomi, Rhizoma Atractylodis macrocephalae, Radix Glycrrhizae, etc.). Methods: Using RP HPLC with Hypersil C 18 column, methanol acetonitrile water acetic acid (10∶22∶70∶1.4,v/v) as mobile phase, detection wavelength at 254nm and p dimethylaminobenzaldehyde as the internal standard.Results: The mean recovery and RSD were 98.2% and 1.9% ( n =6), respectively, the linear range of cinnamic acid was 8.4～168?g?mL -1 ( r =0.9999). Conclusion: The method is simple, rapid, accurate and reproducible, and may be used for the determination of cinnamic acid in Lingguizhugan Decoction.

Tetrazanbigen (TNBG) is a novel synthetic antitumor drug with significant antitumor effects on common solid tumors in vitro and in vivo. It may lead to death of cancer cells through a tumor-associated lipoidosis mechanism, and result in lipid droplets (LDs) accumulation at the cytoplasm. In this study, the effects of TNBG on protein expression in human hepatocellular carcinoma cell line QGY-7701 were studied for elucidating its antitumor mechanism. The proteins extracted from TNBG-treated human hepatocellular carcinoma cell line QGY-7701 were analyzed and compared with control cells by two-dimensional gel electrophoresis. The differential proteins were identified by matrix-associated laser desorption ionization time-of-flight mass (MALDI-TOF-MS) spectrometry. Two proteins of interest, the levels of which were significantly increased in TNBG-treated cells, were further characterized by Western blot analysis. The results showed a total of 846+/-23 spots in control cells and 853+/-30 spots in TNBG-treated cells. Twenty-six up-regulated or down-regulated proteins were found by analyzing differential proteomic 2-DE map. Eleven of them were identified by mass spectrometry. They were protein disulfide-isomerase precursor, 94 kD glucose-regulated protein, heat shock protein (HSP) 90-alpha, ATP-citrate lyase, HMG-CoA reductase, glucose-6-phosphate 1-dehydrogenase, very-long-chain specific acyl-CoA dehydrogenase, squalene synthetase, sterol regulatory element-binding protein 1, fructose-bisphosphate aldolase A, and peroxiredoxin-1. These up-regulated or down-regulated proteins are mostly related to lipid metabolism. The TNBG antitumor mechanism is probably to influence tumor lipid metabolism, resulting in accumulation of LDs in tumor cells.
Antineoplastic Agents/*pharmacology ; Azo Compounds/*pharmacology ; Carcinoma, Hepatocellular/*pathology ; Cell Line, Tumor ; Gonanes/*pharmacology ; Liver Neoplasms/*pathology ; Proteins/*metabolism ; Proteome

d per-oxiredoxin-1. These up-regulated or down-regulated proteins are mostly related to lipid metabolism. The TNBG antitumor mechanism is probably to influence tumor lipid metabolism, resulting in accu-mulation of LDs in tumor cells.