Acteoside

The anti‑inflammatory action of acteoside works by blocking the NF‑κB pathway. It prevents IκB‑α phosphorylation and degradation, and stops NF‑κB p65 from moving into the nucleus. As a result, key pro‑inflammatory genes (TNF‑α, IL‑1β, IL‑6, COX‑2, iNOS) are down-regulated.
To counter oxidative damage, it both reduces ROS generation and enhances cellular defenses—by scavenging radicals, chelating metal ions, and increasing GST activity.
Against cancer cells, acteoside employs varied mechanisms across different signaling pathways, inhibiting growth or triggering apoptosis depending on the context. These are summarized in Fig.1.

Fig. 1 Acteoside's neuroprotective effects. (Mohammed RA.; et al. 2023)

Renal fibrosis represents the ultimate pathological alteration in kidney diseases and is also recognized as a critical factor in the progression of diabetic nephropathy (DN) to renal failure. In their study investigating the protective effects of acteoside against renal interstitial fibrosis—induced in DN rats through intraperitoneal injection of streptozotocin (STZ) combined with unilateral nephrectomy—and its underlying mechanisms, Zhou et al. discovered that acteoside could regulate reactive oxygen species (ROS), autophagic flux and lysosomal function in diabetic nephropathy mice. This could reduce oxidative tubular injury and delay renal interstitial fibrosis in DN mice, which was related to the antioxidant activity of acteoside and its regulation of the autophagy-lysosome pathway.

Fig. 2 The mechanism underlying the inhibitory effect of acteoside on fibrosis progression in diabetic nephropathy. (Zhou M.; et al. 2024)