AIM: To establish HPLC method for the determination of berberine hydrochloride in Huanglianshangqing Tablets(Rhizoma Coptidis, Radix et Rhizoma Rhei, Fructus Forsythiae, etc.). METHODS: The Diamonsil TM C 18(20cm?4.6mm,5?m) was used with 0.033mol?L -1 Potassium dihydrogen phosphate solution-acetonitrile (70∶30) as a mobile phase. The flow rate was 1.0 mL?min -1. The detecting wavelength was 265nm. RESULTS: The linear of berberine hydrochloride was in the range of 0.2376～ 0.5544?g, r= 0.9999. The average recovery was 98.7% and RSD was 0.7%(n=5), respectively. CONCLUSION: The method is simple,rapid and accurate.

Objective To investigate the effect of dexmedetomidine pretreatment on Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway during myocardial injury induced by liver ischemia-reperfusion (I/R) in rats.Methods Twenty-four healthy adult male SpragueDawley rats,aged 8-10 weeks,weighing 220-250 g,were divided into 3 groups (n=8 each) using a random number table method:sham operation group (group S),liver I/R group (group I/R),and dexmedetomidine pretreatment group (group D).The portal vein,superior and inferior vena cava,subhepatic inferior vena cava and hepatic artery were clamped,and the liver was perfused with 4 ℃ lactated Ringer's solution for 60 min through the portal vein to establish the model of liver cold I/R in anesthetized rats.Dexmedetomidine 100 μg/kg was intraperitoneally injected at 30 min before ischemia in group D.Blood samples were collected at 8 h of reperfusion from the inferior vena cava for determination of serum cardiac troponin Ⅰ (cTnⅠ) and heart-type fatty acid binding protein (H-FABP) concentrations (using the automatic biochemistry analyzer),tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 protein (HMGB1) concentrations (by enzyme-linked immunosorbent assay).The rats were then sacrificed,andhearts were harvested for examination of histopathological changes (with a light microscope) and for determination of the malondialdehyde (MDA) content (using thiobarbituric acid method) and superoxide dismutase (SOD) activity (by xanthine oxidase method),and expression of phosphorylated STAT1 and STAT3 (p-STAT1,p-STAT3) and phosphorylated JAK2 (p-JAK2) in myocardial tissues (by Western blot).Results Compared with group S,the serum concentrations of cTnI,H-FABP,TNF-α and HMGB1 were significantly increased,the MDA content was increased,the SOD activity was decreased,and the expression of p-JAK2,p-STAT1 and p-STAT3 was up-regulated in I/R and D groups (P＜0.05).Compared with group I/R,the serum concentrations of cTnI,H-FABP,TNF-α and HMGB1 were significantly decreased,the MDA content was decreased,the SOD activity was increased,the expression of pJAK2,p-STAT1 and p-STAT3 was down-regulated (P＜0.05),and pathological changes of myocardium were significantly attenuated in group D.Conclusion The mechanism by which dexmedetomidine pretreatment mitigates myocardial injury induced by liver cold I/R may be related to inhibiting activation of JAK/STAT signaling pathway in rats.