Na Zhao, Xiaoguang Zhou, Huiling Zhou and Xiangdong Liu
Tong Wu, Guanhua Wang, Caihong Shi, Jinghan Li, Na Zhao, Zihao Dong, Weisan Pan and Xiangrong Zhang
The purpose of this study was to prepare a mosapride citrate-resin (Amberlite® IRP 88) complex and orally fast-disintegrating tablets of the resin complex. The resinate complex of mosapride-Amberlite® IRP 88, mass ratio 2:1, was prepared in an ethanol-water solution. The effects of alcohol concentration, temperature, and pH of the solution on complex formation were evaluated. The complex physicochemical properties were characterized by differential scanning calorimetry, X-ray diffraction and scanning electron microscopy. Orally disintegrating tablets were prepared by direct compression and were optimized using the response surface method. Optimized orally fast-disintegrating tablets disintegrated within 18 s. The pH dependence of mosapride release from the tablet decreased drug dissolution in simulated saliva, whereas it promptly released in the pH 1.0 solution. The data reported herein clearly demonstrate that tablets containing the mosapride-Amberlite® IRP 88 complex for oral disintegration could be particularly useful for patients with swallowing difficulties.
Jing Shen, Chao Wang, Jia-Li Zhang, Zhao Liu, Mi Liu, Jie Yan, Xiao-Rong Chang and li-Na Guo
Objective: To investigate the influence of electroacupuncture (EA) preconditioning at Nei Guan point (PC6) on the opening of mitochondrial permeability transition pore (MPTP) of rabbits with myocardial ischemia-reperrfusion injury, and its underlying mechanism that protects myocardium from injury.
Methods: 18 New Zealand rabbits were randomly assigned to pseudo-operation, model and EA groups， 6 in each group. Setting up models by ligation of coronary artery and electrically stimulating the rabbits in EA group 20 min per day in 5 days before modeling. Testing the activity of serum SOD with the method of actinochemistry, testing changes of mitochondrial transmembrane potential of myocardial cells with the method of synchronous spectrometry, using spectrophotometry to test the changes of the absorption of mitochondria at the spectrum of 520nm to check the opening of MPTP, and testing the apotosis of cells by means of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL).
Results: Compared with model groups, the SOD activity of myocardial cells was significantly enhanced, and the apotosis index (AI) was reduced（P＜0.01），mitochondrial transmembrane potential was significantly increased （P＜0.05），absorption of mitochondria was significantly decreased（P＜0.01).
Conclusion: EA can remarkably improve myocardial ischemia - reperfusion injury, and protect myocardium.
Gongwen Liang, Na Li, Liping Ma, Zhonglian Qian, Yuwen Sun, Luwen Shi and Libo Zhao
The aim of this study was to identify an effective flavonoid that could improve the intracellular accumulation of ritonavir in human brain-microvascular endothelial cells (HBMECs). An in vivo experiment on Sprague-Dawley rats was then designed to further determine the flavonoid’s impact on the pharmacokinetics and tissue distribution of ritonavir. In the accumulation assay, the intracellular leve l of ritonavir was increased in the presence of 25 mmol L−1 of flavonoids in HBMECs. Quercetin showed the strongest effect by improving the intracellular accumulation of ritonavir by 76.9 %. In the pharmacokinetic study, the presence of quercetin in the co-administration group and in the pretreatment group significantly decreased the area under the plasma concentration-time curve (AUC 0–t) of ritonavir by 42.2 % (p < 0.05) and 53.5 % (p < 0.01), and decreased the peak plasma concentration (c max) of ritonavir by 23.1 % (p < 0.05) and 45.8 % (p < 0.01), respectively, compared to the control group (ritonavir alone). In the tissue distribution study, the ritonavir concentration in the brain was significantly increased 2-fold (p < 0.01), during the absorption phase (1 h) and was still significantly higher (p < 0.05) during the distribution phase (6 h) in the presence of quercetin.