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1.
Chinese Journal of Clinical Pharmacology and Therapeutics ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-677123

ABSTRACT

Aim To investigate the possible mechanism of human promyelocytic leukemia cells differentiation and apoptosis induced by all trans_retinoic acid (ATRA) and Ara_c. Methods The effects of ATRA and Ara_c on the tolomerase activity of HL_60 cells were detected by PCR_ELISA. Results The tolomerase activity of HL_60 cells declined during the course of differentiation and apoptosis induced by ATRA and Ara_c. Conclusion These findings suggest that ATRA and Ara_c can inhibit tolomerase activity of HL_60 cells. It may be one of the important mechanisms of human promyelocytic leukemia cells differentiation and apoptosis induced by ATRA and Ara_c.

2.
Chinese Pharmacological Bulletin ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-679208

ABSTRACT

This review introduced the anti-tumor effects of non-steroid anti-inflammatory drugs (NSAIDs) and summarized their possible molecular mechanisms according to recent abroad literatures and our research results. Some evidence showed that the anti-tumor mechanisms of NSAIDs were different in various tumors.NSAIDs decreased the biosynthesis of PGE_2 and regulated the expressions of downstream correlated genes and proteins through restraining abnormal expression of COX-2 in certain neoplasms,which resulted in the inhibition of tumor angiogenesis and proliferation as well as induced apoptosis. But in other cancer cells, NSAIDs, as activators of peroxisome proliferator-activated receptor ? (PPAR?), induced COX-2 expression, promoted the biosynthesis of cyclopentenone prostaglandins (cyPGs). cyPGs further induced tumor cell apoptosis with PPAR? dependently or PPAR? independently. Since their special mechanisms of anti-proliferation and pro-apoptosis, NSAIDs revealed significant synergistic effects with other anti-tumor treatments.

3.
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-673522

ABSTRACT

AIM: To observe the synergetic analgesic effects of low dose of haloperidol, a dopamine antagonist and under-threshold dose of morphine on mice induced by thermal and acetic acid, and to analyze the major mechanism of their synergetic actions. METHODS: To examine the analgesic synergetic effect of haloperidol (0.315 mg/kg, 0.625 mg/kg, 1.25 mg/kg, ip respectively), morphine (3.125 mg/kg, 6.25 mg/kg, 12.5 mg/kg ip, respectively) or combining effect of haloperidol (0.3125 mg/kg) with morphine (3.125 mg/kg) on mice, we compared the change of pain threshold stimulated by thermal, latent period of twisting, the number of times of twisting by acetic acid, and we also estimated the antagonistic effect of d -amphetamine (10 mg/kg) and naloxone (5 mg/kg) on haloperidol and morphine group. RESULTS: Combination of haloperidol with morphine significantly enhanced pain threshold of mice induced by thermal, prolonged latent period of twisting and decreased the number of times of twisting. Naloxone markedly antagonized the combination of analgesic action of haloperidol and morphine and not d -amphetamine. CONCLUSION: Combination of haloperidol with morphine have synergetic analgesic effect and morphine is the dominant factor.

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