Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Yuk-Hap-Tang (YHT) induces cell death in human cervical carcinoma HeLa cells. Caspase-3, -6 and -9 were markedly activated in HeLa cells treated with YHT. The preferred substrate for caspase-3 cysteine protease, PARP, was cleaved to its 85-kDa cleavage product. YHT increased the amount of the anti-apoptotic protein, Bcl-2, and the pro-apoptotic protein, Bax. Although p53 has been reported to accumulate in cancer cells in response to anticancer agents, the p53 expression level was not changed in HeLa cells treated with YHT. Manganese (Mn)-TBAP, a mitochondria-specific SOD mimetic agent and NAC/GSH (N-acetyl cysteine/ reduced glutathione) reduced the YHT-induced cytotoxicity and decreased the number of the YHT-induced apoptotic cells. Furthermore, YHT reduced the expression of Mn-SOD protein and its activity in HeLa cells. The data demonstrate that YHT induces the apoptosis of human cervical carcinoma HeLa cells by intervening Mn-SOD.
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PMID:Yuk-Hap-Tang induces apoptosis by intervening mn-SOD in human cervical carcinoma HeLa cells. 1567 94

In this study, transient forebrain ischemia was induced in male Wistar rats with subsequent 3 days of reperfusion (ischemia/reperfusion group) or 2 days of reperfusion followed by 5 min ischemia and another 1 day of reperfusion (postconditioning group) to assess an effect of delayed postconditioning applied two days after a previous lethal ischemic attack. We have examined immunoreactivity of antioxidant enzymes (MnSOD, CuZnSOD) and proteins related to apoptosis development (Bcl-2, Bax). Results of microdensitometric measurements from the vulnerable hippocampal CA1 region and relatively resistant dentate gyrus were compared to sham controls and identically, results of postconditioning group were compared to ischemic one. Our findings show protective effects of postconditioning in both brain regions examined, include increased expression of antioxidant enzymes, mainly CuZnSOD, what can be demonstrated by microdensitometric results: CuZnSOD density after ischemia and reperfusion was 6261.5 +/- 411.35; after postconditioning 9746.6 +/- 584.55. In addition, postconditioning prevents an excessive ischemia-induced increase of pro-apoptotic protein Bax (Bax density after ischemia and reperfusion was 3462.51 +/- 321.66; after postconditioning 1766.89 +/- 255.63).
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PMID:Ischemic postconditioning in the rat hippocampus: mapping of proteins involved in reversal of delayed neuronal death. 2042 51