Fig. 1: RIP3 was activated to inhibit autophagy in septic AKI mice. | Cell Death & Disease

Fig. 1: RIP3 was activated to inhibit autophagy in septic AKI mice.

From: RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury

Fig. 1

A Kidney tissues were collected from C57BL/6 mice treated with LPS or sterilized saline (con) for immunoblot of phosphorylated RIP3 (p-RIP3, a marker of RIP3 activity) and total RIP3. p-RIP3 and RIP3 expression, against β-actin expression, were increased in the kidneys of LPS-induced mice (n = 3). B Immunoblot showed an accumulation of the expression of LC3II (marker for autophagosome) and p62 (substrate for autophagy) in the kidneys of LPS-induced mice (n = 3). C C57BL/6 mice were treated with sterilized saline (con), LPS, or LPS plus GSK’872 (GSK) for 12 h. Immunoblotting showed that GSK attenuated the increased p-RIP3 in the kidneys of LPS-induced mice (n = 3). D C57BL/6 mice were treated with sterilized saline (con), LPS, or LPS plus GSK for 24 h. Immunoblot showed that GSK attenuated the accumulated LC3II and p62 in the kidneys of LPS-induced mice (n = 3–4). *P < 0.05.

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