N6-(2-Hydroxyethyl)adenosine can suppress TGF-β1 or LPS-induced TGF-β1/Smad and NF-κB signaling pathways in vitro. The levels of ECM production, indicated by expression of collagen I, α-SMA and Fibronectin, are significantly reduced by treatment with N6-(2-Hydroxyethyl)adenosine dose-dependently (5, 10, and 20 μg/ml). Similarly, TGF-β and LPS stimulate increased levels of TNF-α, IL-1β and IL-10. N6-(2-Hydroxyethyl)adenosine treatment reduces the elevated levels of TNF-α and IL-1β and increases IL-10 secretion dose-dependently [1].

Injury of Kidney Tissue in UUO Mice Ameliorated by Intraperitoneal Administration of N6-(2-Hydroxyethyl) adenosine (2.5, 5, and 7.5 mg/kg; intraperitoneal injection). N6-(2-Hydroxyethyl) adenosine treatment prevents the accumulation of fibrosis-related proteins (TGF-β1, α-SMA, collagen I, and Fibronectin) and inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-10) associated with renal interstitial fibrosis. N6-(2-Hydroxyethyl) adenosine could block the accumulation of M1 macrophages, and induced the accumulation of M2 macrophages in ligated kidneys [1].