PMC:4277126 / 21912-22612 JSONTXT

{"project":"NEUROSES","denotations":[{"id":"T505","span":{"begin":109,"end":120},"obj":"CHEBI_22586"},{"id":"T506","span":{"begin":168,"end":171},"obj":"CHEBI_32402"},{"id":"T507","span":{"begin":236,"end":242},"obj":"PATO_0001020"},{"id":"T508","span":{"begin":480,"end":489},"obj":"PATO_0001997"},{"id":"T509","span":{"begin":505,"end":512},"obj":"CHEBI_24996"},{"id":"T510","span":{"begin":543,"end":552},"obj":"PATO_0000470"},{"id":"T511","span":{"begin":553,"end":556},"obj":"CHEBI_29101"},{"id":"T512","span":{"begin":571,"end":575},"obj":"CHEBI_29108"}],"text":"Summary of the anti-aging and antioxidative effectsof LBPs\nIn summary, LBPs have shown potent anti-aging and antioxidant activities (Figure 3). They increase SOD, GPx, CAT, and GR activities, thereby inhibiting oxidative stress-induced damage. LBPs ameliorate oxidative stress-induced cellular apoptosis. They can delay angiotensin II-induced aging of HUVECs by downregulating the expression of p53 and p16. In the ischemia/reperfusion (I/R) injuries to heart, LBPs significantly decreased the myocardium lactate dehydrogenase (LDH) level and increased Na+/K+-ATPase and Ca2+-ATPase activities. LBPs ameliorate oxidative stress-induced cellular apoptosis by downregulating Bax and upregulating Bcl-2."}