ABSTRACT
This paper reported a case of schizophrenia combined with pulmonary tuberculosis treated with clozapine in combination with rifampicin. Due to the induction of hepatic drug enzyme of rifampicin, plasma concentration of clozapine could not reach the effective concentration and the patient still had psychotic symptoms such as persecutory delusion. After discontinuation of rifampicin, plasma concentration of clozapine were in the effective concentration range and the patient's psychiatric symptoms improved. By analysing the therapeutic regimen for the patient with schizophrenia combined with pulmonary tuberculosis, this case suggested a possible interaction between clozapine and rifampin, and provided a reference for the treatment of this type of patients.
ABSTRACT
[ ABSTRACT] AIM:To investigate the protective effect of naringin ( Nar) on the injury of human umbilical vein endothelial cells ( HUVECs) induced by 33 mmol/L high glucose ( HG) and to explore its possible mechanisms.METH-ODS:The injury model was established by treating HUVECs with HG medium for the indicated time (6, 12, 24, 48 and 72 h) , and then the levels of NO, eNOS and p-eNOS were detected, respectively.The effects of Nar on high glucose-in-duced endothelial cell injury were observed.HUVECs were treated with Nar at concentrations of 5, 10, 25, 50 and 100 mg/L for 6 h, 12 h, 24 h, 36 h and 48 h.The levels of NO in the supernatants were measured.The effects of Nar on HG-injured HUVECs were explored by treating the cells with 10 μmol/L of LY294002, a PI3K inhibitor, or 0.5 μmol/L of AKT inhibitorⅣ, an AKT inhibitor, and then the levels of NO, PI3K, AKT, eNOS and their phosphorylated proteins were determined by Western blot.RESULTS:Nar at concentration of 50 mg/L significantly attenuated the injury of endothelial cells induced by high glucose ( P<0.01) , and the protective effects of Nar were abolished by pretreating with the inhibitor of PI3K or AKT (P<0.01).CONCLUSION: Nar protects endothelial cells against the injury induced by high glucose through PI3K/AKT/eNOS pathway.