Substance P Promotes Liver Sinusoidal Endothelium-Mediated Hepatic Regeneration by NO/HGF Regulation.

Liver sinusoidal endothelial cells (LSECs) are highly specialized and involved in hepatic regeneration by interacting with hepatic stellate cells (HSCs) and hepatocytes in a paracrine manner. However, hepatic injury can impair cellular activity and lead to endothelial dysfunction, eventually inducing the development of critical hepatic disease, including cirrhosis. Because LSECs exert their effects through paracrine factors, maintenance of paracrine potentials and survival activity in LSECs under injury stress is a critical strategy for inhibiting disease progression.

Substance P blocks ethanol-induced hepatotoxicity.

Aims: Excessive alcohol consumption induces hepatic injury and promotes lipid accumulation, events involved in the pathogenesis of serious conditions such as alcoholic liver disease (ALD). Thus, protection of hepatocytes against alcohol-induced death is considered to be a critical approach to prevent development of liver disease. Substance P (SP) is capable of promoting cell proliferation and blocking cell death under diverse stresses, leading to beneficial effects in severe diseases, and is therefore likely to have a therapeutic application in hepatic injury.

Substance P prevents development of proliferative vitreoretinopathy in mice by modulating TNF-α.

Purpose: Proliferative vitreoretinopathy (PVR) is an inflammatory fibrotic disease resulting from the inflammatory milieu after retinal detachment, which can prevent retinal healing. This study aimed to elucidate the effect of substance P (SP) on retinal degeneration caused by retinal detachment in vivo and to examine the role of SP in the tumor necrosis factor-alpha (TNF-α)-induced epithelial-mesenchymal transition (EMT) of human RPE cells in vitro.

Methods: PVR-like retinal damage was induced by intravitreally injecting dispase into mice, and SP was systemically injected twice a week for 3 weeks.