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Biomedical subjects

Kazuhiro Nishikawa

Publications and source records attributed to Kazuhiro Nishikawa.

21 records · Page 2Linked to original sources

Soluble complement receptor type 1 protects rats from lethal shock induced by anti-Crry antibody following lipopolysaccharide priming.

BACKGROUND: In rats primed with a trace amount of lipopolysaccharide (LPS), acute lethal shock is induced following the injection of monoclonal antibody against a membrane inhibitor of complement (anti-Crry). Administration of cobra venom factor to exhaust complement before the LPS priming can prevent the lethal reaction. Therefore, we evaluated whether soluble complement receptor type 1 (sCR1), which inhibits complement reaction, can interfere with lethal shock when administered after LPS priming or even after anti-Crry injection. METHODS: sCR1 was administered intravenously before or after the administration of anti-Crry, and the effects on blood pressure and acute lethality were determined. RESULTS: Administration of sCR1 could rescue rats from lethal shock even when it was administered after anti-Crry injection, which immediately causes a blood pressure decrease leading to lethal shock. CONCLUSION: sCR1 may be an effective treatment for acute shock involving complement activation.

Animals↗

Induction of apoptosis in a human breast cancer cell overexpressing ErbB-2 receptor by alpha-tocopheryloxybutyric acid.

The overexpression of ErbB-2 receptor relates to malignant transformation of breast cancer. The present study was carried out to establish the usefulness of alpha-tocopheryloxybutyric acid (TE) as a chemotherapeutic agent for human breast cancer. TE caused induction of apoptosis in MDA-MB-453 cells overexpressing the ErbB-2 receptor. TE reduced levels of activated ErbB-2 receptor and Akt. In contrast, TE induced the activation of p38, and SB203580, a specific inhibitor for p38, attenuated the TE-induced apoptosis. These data indicate that simultaneous occurrences of Akt inhibition and p38 activation by TE result in the cell death.

Apoptosis↗