ABDELAZIZ ADAM IDRISS ARBAB^1,3,#, CHUNQING YIN^4,#, XUBIN LU¹, YAN LIANG¹, ISMAIL MOHAMED ABDALLA¹, AMER ADAM IDRIS³, TIANLE XU^1,2, YONGJIANG MAO¹, ZHANGPING YANG^1,2,*

BIOCELL, Vol.46, No.11, pp. 2443-2454, 2022, DOI:10.32604/biocell.2022.020865

Abstract Mastitis is a common inflammatory cow mammary infection; that causes significant economic loss in dairy industry. Given the interesting connection between metformin’s anti-inflammatory function and mastitis model induced by LTA in pbMECs, our objective was to prove that metformin was beneficial in suppressing proinflammatory response induced by LTA through modulation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways and activation of peroxisome proliferator-activated receptor-γ (PPARγ) in pbMECs. The proliferation of cells and mRNA expression were measured using EdU assay and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Immunoblotting and immunofluorescence analysis were conducted to evaluate the… More >

Tao Wang, Fan Shi, JiQuan Wang, Zi Liu, Jin Su

Oncology Research, Vol.28, No.9, pp. 969-970, 2020, DOI:10.3727/096504022X16414984936773

Abstract Kallistatin has been recognized as an endogenous angiogenesis inhibitor and exerts pleiotropic effects in inhibiting tumor growth, migration, apoptosis, and inflammation. The purpose of the present study was to investigate the potential role and mechanisms of kallistatin in cervical cancer. We demonstrated that kallistatin effectively inhibited cell proliferation and enhanced apoptosis in a dose-dependent manner. Additionally, kallistatin suppressed migration and invasion activities and markedly reduced the expression of matrix-degrading metalloproteinases, progelatinase (MMP-2), MMP-9, and urokinase-type PA (uPA). Kallistatin reversed the epithelial–mesenchymal transition (EMT) and caused the upregulation of epithelial markers such as E-cadherin and inhibited mesenchymal markers such as N-cadherin… More >