Isochlorogenic Acid C Restrains Erk/JNK/NF-κB Signaling to Alleviate Inflammatory Response and Promote Cell Apoptosis

Abstract

Isochlorogenic acid C (ICAC) is found in a variety of natural foods and medicinal plant materials. This study aims to validate the biological activity of isochlorogenic acid C in limiting inflammation by the Erk/JNK/NF-κB pathway. In this study, TNF-α-induced human fibroblast-like synoviocytes and collagen-induced arthritis animal models were used to perceive the potential anti-inflammation mechanism of ICAC. The role of isochlorogenic acid C was evaluated by observing the migration, invasion ability, and apoptotic activity of TNF-α-induced fibroblast-like synoviocytes cells in humans and analysing foot swelling, joint index, and histopathological changes in a collagen-induced RA animal model. The results reveal that ICAC inhibited the proliferation of human fibroblast-like synoviocytes and promoted their apoptosis. ICAC also blocked the nuclear transfer of NF-κB, Erk, and JNK. It was observed that ICAC significantly inhibited the degree of posterior foot swelling in CIA, reducing arthritis scores, bone tissue injury, and articular synovitis. ICAC may promote cell apoptosis and inhibit the hyperactivation of inflammatory cells to alleviate inflammation-induced synovial proliferation through the Erk/JNK/NF-κB pathway.