MAL gene expresses in the mediate and late stage of T-lymphocytes.Many studies have shown that the expression of MAL gene has down regulation or loss in many kinds of tumors including esophageal carcinoma,gastric cancer,colon cancer,head and neck squamous cell carcinoma,and so on.MAL gene is related with the process of generation and development of the tumors.The application of MAL gene for clinical diagnosis,prognostic and instructing therapy needs further studies.

OBJECTIVE:To study the dermal pharmacokinetic difference of triptolide in normal and diabetic rats,and to pro-vide reference for rational drug use in the clinic. METHODS:12 Wistar rats were randomly divided into normal group and diabetic model group(0.1%streptozotocin intraperitoneally),with 6 rats in each group. Both group were given Triptolide cream 0.5 g to ab-dominal skin,and dialysate was collected by microdialysis every 30 min for consecutive 12 h. Subcutaneous concentration was de-tected by HPLC-MS,and subcutaneous concentration-time curves were analyzed and compared between two groups,and Winnon-lin 5.0.1 software was used to calculate pharmacokinetic parameters. RESULTS:The pharmacokinetic parameters of normal group and diabetic model group were that cmax were(1.54±0.37)and(5.12±1.34)μg/ml;tmax were(7.32±0.24)and(6.21±0.35)h;AUC0-12 h were (12.65 ± 4.64) and (37.43 ± 5.23)μg·h/ml,with statistical significance (P<0.05). CONCLUSIONS:The change of dermal structure caused by diabetes can increase percutaneous penetration amount of triptolide in rats,and drug dosage should be reduced according to circumstances so as to reduce side effects.

This paper summarizes the current situation and problems of the research on the theory of "Taibai Seven Medicines" through literature summary and surveys. Although the "Four Beams and Eight Pillars" theory of compounding has a long history, the current research progress of "Taibai Seven Medicines" is mostly focused on plant resources. There lacks researches on the theory of compounding, or development of compounding and large varieties based on "Taibai Seven Medicines". We call for the inheritance and protection of folk experience, and hope that the "Four Beams and Eight Pillars" theory can guide the application and development of the seven Taibai medicines. Therefore, increasing the research on the theory and teaching in undergraduate courses formulary in Chinese medicine are necessary in our province.

Objective:To investigate the role of miR-144-3p in cisplatin resistance of bladder cancer.Methods:Bladder cancer T24 cells were cultured in vitro and divided into blank group (untreated), mimetic control group, miR-144-3p mimetic transfection group, inhibitor control group, and miR-144-3p inhibitor transfection group. Real time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to verify the transfection effect, methyl thiazolyl tetrazolium (MTT) method was used to detect the survival rate of cells treated with cisplatin in each group, and Western blot was used to detect the expression of the target protein. The targeting relationship between miR-144-3p and nuclear factor E2 related factor 2 (Nrf2) was validated using dual fluorescence reporter gene experiments. Furthermore, Nrf2 was knocked out in each group of cells, and the mRNA and protein expression levels of HO-1, Bcl-2, and Caspase-3 were detected by qRT-PCR and Western blot in each group of cells.Results:Compared with the control group, bladder cancer cells in the miR-144-3p mimetic transfection group were more sensitive to cisplatin, while the miR-144-3p inhibitor transfection group had the opposite effect; The miR-144-3p simulant transfection group can effectively inhibit the mRNA and protein expression level of Nrf2 in bladder cancer cells (all P<0.05), while the miR-144-3p inhibitor transfection group can up regulate the mRNA and protein level of Nrf2 (all P<0.05). The miR-144-3p mimetic transfection group showed significant downregulation of mRNA and protein expression of HO-1 and Bcl-2, while the expression of Caspase-3 was upregulated (all P<0.05), while the miR-144-3p inhibitor transfection group showed the opposite results. The luciferase results confirmed that miR 144 3p can directly bind to the 3′- UTR region of Nrf2, reducing the mRNA level of Nrf2. When Nrf2 was knocked out, whether miR-144-3p mimetic transfection group or miR-144-3p inhibitor transfection group, the mRNA and protein expression levels of HO-1, Bcl-2 and Caspase-3 did not change significantly, and miR-144-3p lost the ability to regulate the cisplatin sensitivity of bladder cancer cells. Conclusions:miR-144-3p targets to regulate the sensitivity of Nrf2 to cisplatin in bladder cancer, and miR-144-3p is expected to become a new target for the treatment of cisplatin resistant or refractory bladder cancer.