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Here, we show that a major mechanism by which PAHSAs protect islets of the NOD mice is by directly preventing and reversing the initial steps of metabolic stress-induced senescence

MiR-200a is involved in regulating redox imbalance, and the suppression of aortic endothelial miR-200a expression under hyperglycaemic conditions increases the expression of kelch-like ECH-associated protein 1 (Keap1), which is linked to Nrf2 binding and leads to the inactivation of Nrf2 antioxidant signalling, thereby inducing diabetic vascular endothelial dysfunction [91]

Data is expressed as mean SD

Panda, K

Pharmacological studies with the serotonin precursor, 5-hydroxytryptophan