The Activation of AMPK/NRF2 Pathway in Lung Epithelial Cells Is Involved in the Protective Effects of Kinsenoside on Lipopolysaccharide-Induced Acute Lung Injury

Figure 7

Kin could protect against LPS-induced lung epithelial cells injury by modulating mitochondrial biogenesis in an AMPK/NRF2 pathway-dependent manner. (a) Cell viability of lung epithelial cells treated with different concentrations of Kin (). (versus 0.1 μM groups). (b) LDH content in medium from LPS-induced lung epithelial cells treated with different concentrations of Kin (). (versus 0.1 μM groups). (c) Cell viability of lung epithelial cells in the indicated groups (). (d) LDH content in medium in the indicated groups (). (e, f) The mRNA levels of Tnf-α and IL-1β in the indicated groups (). (g, h) The markers of oxidative stress in the indicated groups (). (i–l) The markers of mitochondrial fusion and fission in the indicated groups (). All data are expressed as the . The significance between these groups was tested, control group and LPS group, LPS group and LPS+Kin group, LPS+Kin group and LPS+Kin+Compound C group, LPS+Kin group and LPS+Kin+NRF2 siRNA group, and LPS+Kin+Compound C group and LPS+Kin+Compound C group+TAT-14. compared with the indicated groups.

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