Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Sep 17;20(18):4607. doi: 10.3390/ijms20184607

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

PKCδ peptide inhibitor attenuates the progression of CCl₄-induced liver fibrosis in mice. (A) Serum aspartate transaminase (AST) and alanine transaminase (ALT) levels from the control, CCl₄, and CCl₄ + V1-1 group mice. (B) The mRNA levels of collagen, iNOS, TNF-α, TLR4, and IL-6 in liver tissue homogenates were measured by qRT-PCR. Each value is the mean ± SD of three experiments. (C) The expression levels of p-PKCδ, SIRT1, and iNOS in the liver tissue were measured by immunoblotting analysis. (D) Liver tissue lysates were subjected to immunoprecipitation with anti-p65 antibodies. Immunoblot analysis was then used to detect the levels of acetyl p65 and total p65 in the immunoprecipitated complexes with anti-acetyl-lysine and anti-p65 antibodies, respectively (upper panel). The lower panel represents immunoblot analysis to detect nuclear p65 levels in liver tissue lysates without immunoprecipitation. (E) Representative liver tissue sections from ND, CCl₄, and V1-1 peptide-treated CCl₄ mice were subjected to immunohistochemical analysis for F4/80, phosphorylated PKCδ, and SIRT1 (upper panel group; original magnification, 200×) and Sirius Red, CK18, and α-SMA (lower panel; original magnification, 100×). * p < 0.05 compared to the control and # p < 0.05 compared to the CCl₄ group. (F) The proposed signaling pathway for liver fibrosis where PKCδ upregulates NF-κB signaling but downregulates SIRT1 signaling simultaneously. In addition, SIRT1 directly downregulates NF-κB through deacetylation.(Red arrow: activation and Blue bar: inhibition).

PKCδ peptide inhibitor attenuates the progression of CCl₄-induced liver fibrosis in mice. (A) Serum aspartate transaminase (AST) and alanine transaminase (ALT) levels from the control, CCl₄, and CCl₄ + V1-1 group mice. (B) The mRNA levels of collagen, iNOS, TNF-α, TLR4, and IL-6 in liver tissue homogenates were measured by qRT-PCR. Each value is the mean ± SD of three experiments. (C) The expression levels of p-PKCδ, SIRT1, and iNOS in the liver tissue were measured by immunoblotting analysis. (D) Liver tissue lysates were subjected to immunoprecipitation with anti-p65 antibodies. Immunoblot analysis was then used to detect the levels of acetyl p65 and total p65 in the immunoprecipitated complexes with anti-acetyl-lysine and anti-p65 antibodies, respectively (upper panel). The lower panel represents immunoblot analysis to detect nuclear p65 levels in liver tissue lysates without immunoprecipitation. (E) Representative liver tissue sections from ND, CCl₄, and V1-1 peptide-treated CCl₄ mice were subjected to immunohistochemical analysis for F4/80, phosphorylated PKCδ, and SIRT1 (upper panel group; original magnification, 200×) and Sirius Red, CK18, and α-SMA (lower panel; original magnification, 100×). * p < 0.05 compared to the control and # p < 0.05 compared to the CCl₄ group. (F) The proposed signaling pathway for liver fibrosis where PKCδ upregulates NF-κB signaling but downregulates SIRT1 signaling simultaneously. In addition, SIRT1 directly downregulates NF-κB through deacetylation.(Red arrow: activation and Blue bar: inhibition).