S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (IMAGE)
Caption
(A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) Immunohistochemistry staining of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) Nissl staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t-test was used for (G). n = 3 or 4. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. #P < 0.05 and ##P < 0.01 versus the TBI group.
Credit
Shuchao Wang, Yating Tan, Minghai Hu, Meijuan Wang, Lu Liang, Xing Luo, Dan Chen, Bing Jiang, Ceshi Chen, Jufang Huang, Kun Xiong
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