Abstract
Diabetes mellitus is a group of physiological dysfunctions associated with hyperglycemia-mediated oxidative stress and apoptosis in pancreatic β-cells. Platycodin D (PLD) is a major saponin isolated from Platycodon grandiflorum that has been reported to possess many pharmacological effects including anti-oxidative, anti-apoptotic and anti-diabetic. In the present study, we evaluated the effects of PLD on oxidative stress and apoptosis in INS-1 cells exposed to streptozotocin (STZ). Our results showed that PLD improved STZ-caused reduction in cell viability of INS-1 cells. PLD prevented STZ-induced apoptosis in INS-1 cells with decreased bax expression and caspse-3 activity, as well as increased bax expression. PLD decreased ROS production and increased SOD activity in STZ-induced INS-1 cells. Treatment with PLD also improved the insulin secretion capacity and the expression of insulin1/2 in STZ-induced INS-1 cells. Furthermore, PLD suppressed the STZ-induced activation of p38 pathway, while enhanced the activation of Nrf2/HO-1 pathway in INS-1 cells. Treatment with p38 agonist (p79350) or knockdown of Nrf2 reversed the protective effects of PLD on INS-1 cells. Taken together, PLD protects INS-1 cells from STZ-induced oxidative stress and apoptosis. The protective effect of PLD might be ascribed to the regulation of p38 and Nrf2 pathways.
Highlights
Diabetes mellitus is a group of physiological dysfunctions with increasing prevalence worldwide (Sreedharan & Abdelmalak, 2018)
The INS-1 cells were exposed to STZ to induce in vitro model of diabetes mellitus
These results suggested that Platycodin D (PLD) inhibited STZ-induced cell apoptosis in INS-1 cells
Summary
Diabetes mellitus is a group of physiological dysfunctions with increasing prevalence worldwide (Sreedharan & Abdelmalak, 2018). Diabetes mellitus is characterized by hyperglycemia, which directly results from insulin resistance, inadequate insulin secretion, or excessive glucagon secretion (Alam et al, 2014; Kreider et al, 2018). Diabetes mellitus remains a life-threatening disease, the available treatment can neither cure nor completely control the complications of this disorder. Hyperglycemia-mediated oxidative stress and apoptosis in pancreatic β-cells have been found to play major role in the development of diabetes mellitus (Lim et al, 2018; Patar et al., 2018; Yao et al, 2017). Preventing the oxidative stress and apoptosis in pancreatic β-cells may contribute to the prevention and treatment of diabetes mellitus
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