IndraLab

Statements


NAC inhibits RIPK1. 6 / 6
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"In our study, NAC and AAP inactivated RIPK1 and RIPK3 that led to the reduction of H 2 O 2 -induced necroptosis (XREF_FIG)."

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"In this study, the addition of NAC effectively reduced EtOH treatment necroptosis of the osteoblastic cells as NAC attenuated the upregulation of RIPK1 and RIPK3 (Figure 6(g))."

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"It has been reported that ROS promotes necroptosis by a positive feedback mechanism in osteoblastic cells, while ROS inhibitor N-acetylcysteine (NAC) attenuates the up-regulation of RIPK1, RIPK3 and MLKL, and the RIP1 inhibitor necrostatin-1 (Nec-1) reduced ROS generation [17]."

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"NAC (ROS inhibitor) inhibited RIP1, RIP3, and increased ATF4; however, necrostatin-1 (Nec-1) (RIP1 inhibitor) specifically inhibited the protein expression of RIP1 and RIP3 and had no influence on ATF4."

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"In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2."

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"Necrostatin-1-mediated treatment effectively inhibits the RIPK1/RIPK3/MLKL-dependent signaling, and NAC partly prevents the production of ROS and decreases the activation of necroptosis through a positive feedback loop involving RIPK1/RIPK3 and finally ameliorates alcohol-induced osteopenia by reducing osteoblast necroptosis."