Mouse MMP2 ELISA Kit

Pharmacological treatments for non-alcoholic steatohepatitis (NASH) are still unsatisfactory. Fibrosis is the most significant predictor of mortality and many anti-fibrotic agents are under evaluation. Herein, we assessed in vitro the effects of the FXR agonist obeticholic acid (OCA) and the dual FXR/TGR5 agonist INT-767 in a well-established co-culture NASH model. Co-cultures of human hepatoma and hepatic stellate (HSCs) cells were exposed to free fatty acids (FFAs) alone or in combination with OCA or INT-767. mRNA expression of HSCs activation markers and FXR engagement were evaluated at 24, 96 and 144 hours. Collagen deposition and metalloproteinase 2 and 9 (MMP2-9) activity were compared to tropifexor and selonsertib. FFAs induced collagen deposition and MMP2-9 activity reduction. Cotreatment with OCA or INT-767 did not affect ACTA2 and COL1A1 expression, but significantly reduced FXR and induced SHP expression, as expected. OCA induced a dose-dependent reduction of collagen and induced MMP2-9 activity. Similarly, INT-767 induced collagen reduction at 96 h and a slight increase in MMP2-9. Tropifexor and Selonsertib were also effective in collagen reduction but showed no modulation of MMP2-9. All tested compounds reduced collagen deposition. OCA exerted a more potent and long-lasting effect, mainly related to modulation of collagen turn-over and MMP2-9 activity.

Cervical cancer is one of the most common women cancers. The tumor screening by nurse care is efficacy for cancer prevention. Serum amyloid A1 (SAA1) has shown to be associated with cervical cancer malignancy. The detail information for SAA1 in cervical cancer has not yet been investigated. IL-1 beta was performed to induce cervical cancer cell lines. Subsequently, SAA1 was silenced or overexpressed in c-33A respectively. The data showed that the expression levels of SAA1 were increased in IL-1 beta induced cervical cell lines. Downregulation of SAA1 reduced cell proliferation, migration and invasion in c-33A cells, whereas overexpression increased, indicating that SAA1 is a tumor promoter in cervical cancer. Also, SAA1 positively regulates the expression of MMP2, MMP7 and MMP9, which is associated with extracellular matrix reproduction. Furthermore, NF-kappa B inhibitor, SC75741, reversed the effects of SAA1 in cervical cancer, revealing that it might be a potential mechanism for SAA1 in cervical cancer. Therefore, SAA1 is a potential biomarker for cervical cancer in the inflammatory microenvironment.