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The purpose of this study was to investigate the protective effect of catalpol on Lipopolysaccharide (LPS)/D-galactosamine (D-gal)-induced acute liver injury in mice. The mouse model was established by injection of LPS and D-gal. Catalpol (2.5, 5, 10 mg/kg) were pretreated intraperitoneally 1 h before LPS and D-gal. The survival rate, AST, ALT, MDA, MPO activity, hepatic tissue histology, TNF-α level, and NF-κB activation were assayed. The results revealed that catalpol dose-dependently elevated the survival rate. Furthermore, catalpol reduced the activities of AST, ALT, MDA, and MPO. The production of TNF-α was also inhibited by treatment of catalpol. In addition, catalpol inhibited LPS/D-gal-induced NF-κB activation. The expression of Nrf2 and HO-1 were up-regulated by treatment of catalpol. These results indicated that pretreatment with catalpol could attenuate LPS/D-gal-induced acute liver injury in mice and the underlying mechanism may due to the inhibition of NF-κB signaling pathway and the activation of Nrf2 signaling pathway.

Colorectal cancer (CRC) remains a primary contributor to cancer-associated mortality. The Lin28/let-7 axis has previously been verified to participate in numerous pathophysiological processes involved in CRC. However, the potential roles and underlying mechanisms of this axis in apoptosis during CRC remain to be fully elucidated. The present study aimed to evaluate the role and reveal the molecular mechanisms of the Lin28/let-7 axis in the apoptosis of CRC cells. An MTT assay was conducted to assess the cell viability of HCT116 and HT29 CRC cells, and caspase-3 activity was analyzed to measure the apoptosis of CRC cells. Western blotting and reverse transcription-quantitative polymerase chain reaction were performed to examine the expression of Lin28, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, Bcl-2-like 1 (BCL2L1) and let-7c. The present study demonstrated that Lin28 was upregulated whereas let-7c was downregulated in CRC tissues and cell lines compared with normal tissues and NCM460 normal colon epithelial cells, respectively. Forced overexpression of let-7c promoted apoptosis in CRC cells, which was at least partially mediated via the targeting of BCL2L1. Furthermore, knockdown of Lin28 decreased viability and promoted apoptosis in CRC cells, whereas this effect was attenuated by let-7c inhibition. The findings of the present study suggest the involvement of the Lin28/let-7c axis in apoptosis during CRC, and indicate the potential role of this pathway as a novel therapeutic target in CRC.

Hepatocellular carcinoma (HCC) was one of the most common cancers around the world, has very low 5-year survival rate. However, the mechanism of HCC occurrence and development is largely unknown. LDB2 belongs to the LIM-domain binding family and functions as an adaptor for transcriptional regulation. Here we found that LDB2 is downregulated in HCC samples. LDB2 has the ability to inhibit proliferation and migration of hepatocarcinoma cells. We found that the proliferation and migration abilities in HCC sample cells were impaired after LDB2 overexpression and vice versa. In mechanism, we found that LDB2 can recruit BRD7 to HEY1 promoter and then block its expression. HEY1 whose expression is upregulated in HCC acts as an oncogene. In brief, our research reveals a new regulatory mechanism for hepatocarcinoma cell proliferation and migration.