ABSTRACT
OBJECTIVE:To observe the efficacy and safety of tripterygium glycosides combined with mizolastine in the treatment of dermatitis and eczema. METHODS:138 patients with dermatitis and eczema were randomly divided into control group (69 cases) and observation group (69 cases). Control group received Mizolastine sustained release tablet 10 mg,orally,once a day. Observation group additionally received Tripterygium glycosides tablet 20-30 mg,orally taking after a meal,3 times a day. All patients treated for 3 weeks,patients’life way remained unchanged during treatment. Clinical efficacy,total score of symptoms, IL-2,IL-6,CRP levels and the incidence of adverse reactions in 2 groups were observed. RESULTS:The total effective rate in observation group was significantly higher than control group,with significant difference (P<0.01). After treatment,the total score of symptoms,IL-2,IL-6,CRP levels in 2 groups were significantly lower than before,and observation group was lower than control group,with significant differences(P<0.05 or P<0.01). The incidence of adverse reactions in observation group was significantly lower than control group,with significant difference (P<0.05). CONCLUSIONS:Tripterygium glycosides combined with mizolastine shows better efficacy than mizolastine alone in the treatment of dermatitis and eczema,with better safety.
ABSTRACT
Objective: To determine the potency of QN-2013, a derivative of quinoxaline 1,4-N-oxide, as a hypoxia-selective cytotoxin or a radiosensitizer. Methods: In vitro cytotoxicity and radiosensitization, as well as in vivo antitumor activity were determined by colony formation and tumor growth delay respectively. The changes in the cell cycle, DNA damage and repair of damaged DNA were assayed by FCM and “comet” assay, separately. Results: ICN250 and ICair50 of QN-2013 for HeLa-S3 cells were 0.08 and 1.7 mmol*L－1 respectively, namely, HCR=21. This suggested that QN-2013 was a fairly hypoxic cytotoxin, but inferior to SR-4233. QN-2013 had an evident radiosensitization either in vitro or in vivo. It was noted, however, that the value of in vitro SERs increased exponentially with increasing concentration of the drug, but the in situ antitumor activity seemed to be independent of doses of the drug. The systemic toxicity of QN-2013 was superior to an LD50 of 265 mg*kg－1 compared with 80 mg*kg－1 for SR-4233. In hypoxic condition QN-2013 induced S retension effect and G2M block in HeLa-S3 cells, caused DNA double strand break, and inhibited the repair of radiation-induced DNA damages. All of these reactivenesses might be involved in the action mechanism of QN-2013. Conclusion: QN-2013 is a fair hypoxia-selective cytotoxin, and has shown improved antitumor activity in vivo in combination with radiation. In general, These results suggest that the series of quinoxaline di-N-oxide derivatives hold out bright prospect for the development of novel bioreductive antitumor drugs.