Fig 2: HA/CD44 axis activated the Akt/mTOR pathway by promoting the expression of ANX A1, which was increased in CP/CPPS patients to promote Th1 cells differentiation. (A) Heatmap revealing the correlation between ANX A1 and several clinical features. (B) ANX A1 increased in CP/CPPS patients. (C) ANX A1 increased in severe NIH-CPSI scores. (D) ANX A1 increased in severe pain symptoms. (E) The differentiation percentage of Th1 cells in the in vitro differentiation experiment among NC + PBS, NC + HA, and shAnxa1 + HA groups. (F) Corresponding data analysis according to data in (E, G) The expression levels of p-mTOR, mTOR, p-Akt, and Akt of Th1 cells in the in vitro differentiation experiment among NC + PBS, NC + HA, and shAnxa1 + HA groups. (H) The possible mechanism of HA/CD44 promoting Th1 cells differentiation. ***p < 0.001, **p < 0.01, *p < 0.05.

Fig 3: RWP significantly restored expression of AnxA1 in LPS-induced inflammation. Primary human monocytes were incubated with RWP 20 μg/mL or RWP 200 μg/mL and activated with 1 μg/mL LPS. Expression of AnxA1 (a) and FPR2 (b) was assessed following 24 h treatment with LPS. Protein expression was quantified by using optical density (O.D.) ratio for AnxA1 or FPR2 versus β-actin; normalized values obtained are reported under western blot images. C: control; L: LPS; R20: RWP 20 μg/mL; R200: RWP 200 μg/mL.