Expression of JNK/SAPK in lung and bronchus of radon-exposed mice / 中华放射医学与防护杂志

Objective To study the expression of JNK/SAPK(c-Jun NH2-terminal kinase/stress activated protein kinase)in lung and bronchus of radon-exposed mice.Methods Male BALB/c mice were exposed to radon and its progeny with the cumulative dose of 0.02,30 or 60 working level month(WLM),respectively.The expression levels of JNK/SAPK in lung and bronchus were determined with Real-Time PCR,Western blot and immunohistochemistry methods.Results The JNK mRNA levels in lung tissues of mice exposed to radon of 30 and 60 WLM were higher than those of the control by 3.56 and 2.96 times,respectively.The relative expression levels of JNK and phospho-JNK proteins were higher than those of the control by using Western blot and immunohistochemistry methods.Condusiom Expose to the radon and its progeny might activate the JNK/SAPK intracellular signaling pathway.

Effect of short-term ethanol on the proliferative response of Swiss 3T3 cells to mitogenic growth factors

Both adaptive and deleterious responses of cells to ethanol are likely triggered by short-term interactions of the cells with ethanol. Many studies have demonstrated the direct effect of ethanol on growth factor-stimulated cell proliferation. Using Swiss 3T3 cells whose growth was inhibited by ethanol in a concentration-dependent manner, we further investigated the molecular mechanisms of acute ethanol treatment by examining its effect on EGF- and PDGF-mediated cellular signaling systems for the mitogenic function. Tyrosine autophosphorylation of the growth factor receptors was partially prevented by ethanol in intact cells. When ethanol was included before or after EGF stimulation, no effect on the receptor signaling was observed. Here we also report that ethanol inhibits activation of ERK induced by both EGF and PDGF. EGF-induced JNK activation was reduced but PDGF-induced rapid JNK activation was delayed by the addition of ethanol. The balance between its inhibitory and stimulatory effect on the signaling molecules might determine the rate of cell growth.

The Role of JNK/SAPK Signaling-Transduction Pathway in the Effect of El-emene Against Hepatocarcinoma / 中国肿瘤生物治疗杂志

Objective:To find out the role of JNK/SAPK signaling-transduction pathway in the effect of elemene against hepatocarcinoma, offering the clue to ilustrate the molecular mechanisms of antitumor effects of elemene. Methods: The detection of the distribution of elemene in Hca-F cells was detected by gas chomatography and apoptotic changes in elemene treated. SMMC7721 cells were examined by TEM. After elemene treatment, the activation of JNK/SAPK in HepG2 cellls and the DAXX gene expression in SMMC7721 cells were detected by Western blotting and RT-PCR respectively. Results: Gas chomatography showed that elemene was detected at 8. 42 minute. The SMMMC7721 cells treated by elemene for 3 hours began to show typical apoptotic changes . The JNK/SAPK activity in HepG2 cell treated with heat shock was the highest of all groups and the group treated with elemene was the next and the control group is the lowest one. There was no DAXX gene expression in SMMC7721 cells treated with elemene. Conclusion: Elemene can diffuse into cells. Tumor cell apoptosis treated with elemene may be induced by JNK/SAPK activating and DAXX signal pathway may not play key role in JNK/SAPK activation induced by elemene.