Dinitropheno (Mouse) IgM ELISA Kit

Currently, many surfactants used in self-emulsifying drug delivery systems (SMEDDS) can cause gastrointestinal mucosal irritation and systemic toxicity. In the present study, SMEDDS were loaded with pueraria flavones, using sodium taurocholate to replace polyoxyl 40 dydrogenated castor oil (Cremophor (R) RH 40) as the surfactant (PF-SMEDDSNR) to reduce the toxicity of SMEDDS using Cremophor (R) RH 40 as the surfactant (PF-SMEDDSR). The absorption rate constants (K-a) and intestinal permeability coefficients (P-eff) were measured. The effects of P-glycoprotein inhibitor (verapamil), adenosine triphosphate (ATP) inhibitor (2,4-dinitrophenol), and carrier inhibitor on K-a and P-eff values in the ileum were determined. Biological safety was also evaluated. The K-a and P-eff values increased for PF-solution concentrations of 200 mu g/ml > 100 mu g/ml > 400 mu g/ml in individual segments of the intestines. The results indicated that P-eff values of PF-SMEDDSNR were distinctly higher than those of SMEDDS loaded with pueraria flavones using Cremophor (R) RH 40 as the surfactant (PF-SMEDDSR) and PF-solution in four intestinal segments. However, the K-a values of PF-SMEDDSNR were higher only in the jejunum and ileum segments compared with those of PF-SMEDDSR and PF-solution. The K-a and P-eff values without verapamil were significantly lower than those with verapamil. 2,4-Dinitrophenol had no effect on K-a and P-eff values. The K-a and P-eff values of PF-SMEDDSNR significantly decreased after perfusing B-SMEDDSNR for 1 h prior to the study. The cell viabilities after exposure to SMEDDSNR were higher than those of SMEDDSR in the range of 81-324 mu g/ml. Lactate dehydrogenase release from cells treated with PF-SMEDDSNR or B-SMEDDSNR was significantly lower than that from cells treated with PF-SMEDDSR or B-SMEDDSR at surfactant concentrations of 243 and 324 mu g/ml. However, there were no differences with SMEDDS treatment at surfactant concentrations of 0-162 mu g/ml. Hence, we conclude that SMEDDS using sodium taurocholate as the surfactant can reduce the toxicity of SMEDDS, meanwhile, maintain the characteristics of SMEDDS, and enhance intestinal absorption.

Pyrazinamide is an anti-tubercular agent, used as a part of a three-drug regime (any three of the following: rifampicin, isoniazid, pyrazinamide, streptomycin or ethambutol) for the initial phase of treatment. One of the effects pyrazinamide has on mammalian cells is to regulate NAD(+)/NADH levels. We have recently found that changes in NAD(+)/NADH are associated with regulation of expression levels of SUR2A, a cardioprotective protein serving as a regulatory subunit of cardiac ATP-sensitive K+ (K-ATP) channels. Here, we have tested whether pyrazinamide regulate expression of SUR2A/K-ATP channel subunits and resistance to metabolic stress in embryonic heart-derived H9c2 cells. We have found that 24-h-long treatment with pyrazinamide (3 mcg/ml) increased mRNA levels of SUR2A, SUR2B and Kir6.1 without affecting mRNA levels of other K-ATP channel subunits. This treatment with pyrazinamide (3 mcg/ml) protected H9c2 cells against stress induced by 10 mM 2,4-dinitrophenol (DNP). The survival rate of DNP-treated cells was 45.6 +/- 2.3% (n = 5) if not treated with pyrazinamide and 90.8 +/- 2.3% (n = 5; P< 0.001) if treated with pyrazinamide. We conclude that pyrazinamide increases resistance to metabolic stress in heart H9c2 cells probably by increasing SUR2A and SUR2B expression. Our results of this study indicate that pyrazinamide should be seriously considered as a drug of choice for patients with tuberculosis and ischaemic heart disease.