Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxalate is not only considered to be one of the main constituents of urinary stones, but it also has toxic effects on renal tubular epithelial cells, affecting the pathogenesis of nephrolithiasis. We tried to elucidate the effects of oxalate on human renal tubular epithelial cells (HK-2 cells). In addition, we investigated whether the toxic effect of oxalate occurs by apoptosis, and determined the expression of Bcl-2 family and caspase 9 proteins known as apoptosis-related protein. HK-2 cells were incubated with different concentrations of oxalate, and the effect of oxalate on the growth of the cells was assessed by MTT assay. A caspase-3 activity assay and TUNEL assay were performed on HK-2 cells after oxalate exposure in order to evaluate apoptosis. Immunoblot analysis of Bax, Bcl-2, Bcl-xL, and caspase-9 were performed. Oxalate exposure resulted in significant growth inhibition of HK-2 cells as oxalate concentrations increased. The toxic effect of oxalate on HK-2 cells was considered to occur through apoptosis, as suggested by the increase of caspase-3 activity. The percentage of positive nuclei stained using the TUNEL method was 18+/-2.3 in oxalate-treated cells and 2.5+/-0.9 in untreated cells (P<0.05). Bax and caspase-9 protein expression increased significantly as oxalate concentrations increased, but Bcl-2 protein expression decreased. There was no difference in Bcl-xL protein expression among the various concentrations of oxalate. Our results show that oxalate has a toxic effect on HK-2 cells and that this effect is induced by apoptosis, which may be mediated by an intrinsic pathway.
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PMID:Apoptosis induced by oxalate in human renal tubular epithelial HK-2 cells. 1575 46

Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with visnagin (IR + visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + visnagin group decreased significantly (P<0.01). In conclusion, visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.
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PMID:Visnagin ameliorates myocardial ischemia/reperfusion injury through the promotion of autophagy and the inhibition of apoptosis. 3290 22