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The treatment of aged rats with an inhibitor of iNOS or the use of GSNO in vitro demonstrated that SIRT1 is inhibited by S-nitrosylation and this results in p53 and NF-B increased activity with consequent production of pro-inflammatory cytokines [99]

Compared with the control, expression of SlBEL11 significantly repressed the promoter activity of SlLCY-b2 (Figure 4B)

Furthermore, side effects such as dose limitations and cardiotoxicity have significantly restricted their clinical application (5)