[Xinfeng capsule inhibits immune inflammation in osteoarthritis by inhibiting the miR- 23a-3p/PETN/PI3K/AKT/mTOR pathway].

OBJECTIVE To observe the inhibitory effect of Xinfeng capsule (XFC) on immune inflammatory response in the coculture system of chondrocytes and CD4+ T cells from patients with osteoarthritis (OA). OBJECTIVE Thirty OA patients and 30 healthy subjects were examined for the expression of miR-23a-3p/PTEN/PI3K/AKT/mTOR. The changes in the miR-23a-3p/ PTEN/PI3K/AKT/mTOR pathway and the clinical indicators of the OA patients after XFC treatment were observed. OA-CD4+ T cells and OA-Chondrocytes cells were cultured in Transwel chambers, and the expressions of miR-23a-3p, PTEN, PI3K, AKT and mTOR mRNA were detected by RT-PCR; the levels of IL-1β, IL-6, IL-10 and TNF-α were detected by ELISA. The protein expressions of PTEN, PI3K, AKT, p-AKT, mTOR and p-mTOR were detected by Western blotting. OBJECTIVE Compared with healthy individuals, OA patients showed significantly increased expressions of miR-23a-3p, PTEN, PI3K, AKT, IL-1β, IL-6 and TNF-α and lowered expressions of PTEN and IL-10 (P < 0.01). Positive correlations were found between miR-23a-3p and IL-6 and between PI3K and IL-10; mTOR was positively correlated with IL-6, IL-10, complement C3 and C4 (P < 0.01 or 0.05). Intervention with XFC obviously down-regulated the expressions of IL-1β, IL-6, and TNF-α and up-regulated the expression of IL-10 (P < 0.01). In the cell co-culture systems, the expressions of miR-23a-3p, PI3K, Akt, mTOR, IL-1β, IL-6 and TNF-α were up-regulated while the expressions of PTEN and IL-10 were down-regulated in the model group (P < 0.01). Overexpression of miR-23a-3p significantly up-regulated the expressions of IL-1β, IL-6, TNF-α, miR-23a-3p, PI3K, AKT and mTOR and lowered the expressions of PTEN and IL-10 (P < 0.01 or 0.05). The expressions of IL-1β, IL-6, TNF-α, miR-23a-3p, PI3K, AKT and mTOR were down-regulated and the expressions of IL-10 and PTEN were up-regulated in XFC-treated cells (P < 0.01 or 0.05). OBJECTIVE XFC can reduce the inflammatory response in patients with OA by down-regulating the expression of miR-23a-3p, inhibiting the activation of the PTEN/PI3K/AKT/ mTOR pathway, and regulating the expression of IL-1β, IL-6, IL-10 and TNF-α.