Diabetes from pancreatic β cell death and insulin resistance is a serious metabolic disease in the world. Although the overproduction of mitochondrial reactive oxygen species (ROS) plays an important role in the pathogenesis of diabetes, its specific molecular mechanism remains unclear. Here, we show that the natural Charisma of Aqua (COA) water plays a role in Streptozotocin (STZ) diabetic stress-induced cell death inhibition. STZ induces mitochondrial ROS by increasing Polo-like kinase 3 (Plk3), a major mitotic regulator, in both Beta TC-6 and Beta TC-tet mouse islet cells and leads to apoptosis. Overexpression of Plk3 regulates an increase in mitochondrial ROS as well as cell death, also these events were inhibited by Plk3 gene knockdown in STZ diabetic stimulated-Beta TC-6 cells. Interestingly, we found that natural COA water blocks mitochondrial ROS generation through the reduction of Plk3 and prevents apoptosis in STZ-treated beta cells. Furthermore, using the 3D organoid (ex vivo) system, we confirmed that the insulin secretion of the supernatant medium under STZ treated pancreatic β-cells is protected by the natural COA water. These findings demonstrate that the natural water COA has a beneficial role in maintaining β cell function through the inhibition of mitochondrial ROS-mediated cell death, and it might be introduced as a potential insulin stabilizer.
Keywords: 3D organoid; 3D, three-dimensional; APC, anaphase-promoting complex; AQP, aquaporin; Apoptosis; COA, Charisma of Aqua; DKD, diabetic kidney disease; Diabetes; MAVS, mitochondrial antiviral signaling protein; MMP, mitochondrial membrane potential; Natural COA water; Pancreatic β-cells; Plk3; Plk3, Polo-like kinase 3; ROS, reactive oxygen species; Reactive oxygen species (ROS); STZ, Streptozotocin; ex vivo; ΔΨm, mitochondrial membrane potential.
© 2022 The Authors.