Manouchehri, N., Khodagholi, F., Dargahi, L., Ahmadiani, A. (2019). Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells. Iranian Journal of Pharmaceutical Research, 18(3), 1445-1455. doi: 10.22037/ijpr.2019.1100711
Nasim Manouchehri; Fariba Khodagholi; Leila Dargahi; Abolhassan Ahmadiani. "Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells". Iranian Journal of Pharmaceutical Research, 18, 3, 2019, 1445-1455. doi: 10.22037/ijpr.2019.1100711
Manouchehri, N., Khodagholi, F., Dargahi, L., Ahmadiani, A. (2019). 'Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells', Iranian Journal of Pharmaceutical Research, 18(3), pp. 1445-1455. doi: 10.22037/ijpr.2019.1100711
Manouchehri, N., Khodagholi, F., Dargahi, L., Ahmadiani, A. Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells. Iranian Journal of Pharmaceutical Research, 2019; 18(3): 1445-1455. doi: 10.22037/ijpr.2019.1100711
Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells
1Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract
Preconditioning (PC) as a protective strategy against noxious insults can decline cell death and apoptosis. It has been approved that mitochondria play a key role in PC mechanism. The critical role of complex I (CI) in oxidative phosphorylation machinery and intracellular ROS production, particularly in the brain, accentuates its possible role in PC-induced neuroprotection. Here, differentiated PC12 cells were preconditioned with ultra-low dose LPS (ULD, 3 μg/mL) prior to exposure to high concentration of LPS (HD, 750 μg/mL). Our results showed that HD LPS treatment reduces cell viability and CI activity, and intensifies expression of cleaved caspase 3 compared to the control group. Intriguingly, PC induction resulted in enhancement of cell 2 viability and CI activity and reduction of caspase3 cleavage compared to HD LPS group. In order to explore the role of CI in PC, we combined the ULD LPS with rotenone, a CI inhibitor. Following rotenone administration, cell viability significantly reduced while caspase3 cleavage increased compared to PC induction group. Taken together, cell survival and reduction of apoptosis followed by PC can be at least partially attributed to the preservation of mitochondrial CI function.
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