International immunopharmacology · 2026
Picrorhiza scrophulariiflora ethanol extract ameliorates CCl4-induced acute liver injury by blocking the TSP1/TNF/NF-κB axis.
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Li Menghao, Ren Fengming, Li Tao, Li Qiongyuan, He Lifen, Li Xuegang, Ye Xiaoli, Ma Hang
Аннотация
AIM OF THE STUDY: This study aimed to investigate the effects and potential mechanisms of Picrorhiza scrophulariiflora ethanol extract (PSE) in ameliorating carbon tetrachloride (CCl4)-induced acute liver injury.
MATERIALS AND METHODS: Mouse models of CCl4-induced acute liver injury and HepG2 cell models were established to assess the pharmacodynamic effects of PSE. The viability of HepG2 cells treated with PSE and CCl4 was determined using CCK-8 assays. H&E staining, liver index, and serum liver function markers were analyzed to evaluate the protective effect of PSE. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were assessed both in vivo and in vitro. Using transcriptomics, we identified key pathways and potential target of PSE. To validate the efficacy of these targets within relevant pathways, we conducted cellular thermal shift assays (CETSA), molecular docking, Western blotting, and quantitative real-time PCR analyses.
RESULTS: Compared with the model group, PSE treatment significantly increased the survival rate of HepG2 cells. PSE markedly improved the general condition of mice, including reduced liver index, decreased levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and ameliorated histopathological damage in liver tissues. Furthermore, PSE significantly increased SOD activity while reducing MDA levels both in vivo and in vitro. Transcriptomics and cellular thermal shift assays indicated that the effects of PSE were mediated through the TSP1/TNF/NF-κB signaling pathway. In addition, PSE treatment decreased both the protein and mRNA levels of NF-κB, TNF-α, IL-6, and IL-1β.
CONCLUSION: PSE exerts anti-inflammatory effects via the TSP1/TNF/NF-κB axis, thereby ameliorating CCl4-induced acute liver injury.
MATERIALS AND METHODS: Mouse models of CCl4-induced acute liver injury and HepG2 cell models were established to assess the pharmacodynamic effects of PSE. The viability of HepG2 cells treated with PSE and CCl4 was determined using CCK-8 assays. H&E staining, liver index, and serum liver function markers were analyzed to evaluate the protective effect of PSE. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were assessed both in vivo and in vitro. Using transcriptomics, we identified key pathways and potential target of PSE. To validate the efficacy of these targets within relevant pathways, we conducted cellular thermal shift assays (CETSA), molecular docking, Western blotting, and quantitative real-time PCR analyses.
RESULTS: Compared with the model group, PSE treatment significantly increased the survival rate of HepG2 cells. PSE markedly improved the general condition of mice, including reduced liver index, decreased levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and ameliorated histopathological damage in liver tissues. Furthermore, PSE significantly increased SOD activity while reducing MDA levels both in vivo and in vitro. Transcriptomics and cellular thermal shift assays indicated that the effects of PSE were mediated through the TSP1/TNF/NF-κB signaling pathway. In addition, PSE treatment decreased both the protein and mRNA levels of NF-κB, TNF-α, IL-6, and IL-1β.
CONCLUSION: PSE exerts anti-inflammatory effects via the TSP1/TNF/NF-κB axis, thereby ameliorating CCl4-induced acute liver injury.