NF-κB/ICAM-1 signaling regulates vascular dysfunction in depressive hypertension rats.

The relationship between depression and hypertension has garnered increasing scholarly attention, particularly regarding the role of depression in exacerbating organ damage in hypertensive individuals. Inflammation is a key characteristic of organ damage associated with elevated blood pressure. However, the specific impact of inflammation on vascular dysfunction in hypertensive rats with depression has yet to be fully understood. This study examines the effects of the NF-κB inhibitor MG132 on blood pressure, depression-like behaviors, endothelial function, and vascular remodeling in hypertensive rats exhibiting depressive symptoms. The administration of MG132 resulted in a significant reduction in blood pressure and an improvement in depressive behaviors among these rats. Furthermore, MG132 treatment led to a notable decrease in serum levels of Angiotensin II (Ang⠡) and Vascular Endothelial Growth Factor (VEGF), while increasing nitric oxide (NO) levels in spontaneously hypertensive rats (SHR) and those with chronic depression. Additionally, MG132 inhibited the differentiation of endothelial progenitor cells (EPCs) into smooth muscle cells (SMCs) and reduced the levels of inflammatory cytokines, including high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). Moreover, MG132 effectively suppressed the expression of NF-κB P65 and its downstream signaling pathway, intercellular adhesion molecule-1 (ICAM-1).