HIIT reversed microglial polarization via the Jak2/Stat3 pathway
in OA rats
To examine the mechanisms by which HIIT would alleviate OA-induced pain
through the Jak2/Stat3 pathway, we activated the Jak2/Stat3 signalling
pathway by intraperitoneal injection of C-A1 in OA rats. Flow cytometry
results confirmed that the CD68 expression of the OA+C-A1 rats was
higher than that of OA rats, but CD163 was lower than that of OA rats
(P < 0.001). The expression levels of CD68 were higher
in the OA+C-A1+HIIT rats than in OA+ HIIT rats, but CD163 was lower than
that of OA+HIIT rats (P < 0.001, Figure 6 A-B).
Subsequently, pain neurotransmitters were measured by WB to determine
whether Jak2/Stat3 pathway could affect their release. Activation of the
Jak2/Stat3 pathway significantly increased the expression of Glu, c-fos,
SP, and IL-6, but HIIT reversed the OA-induced increase. The expression
levels of Glu, c-fos, SP, and IL-6 were significantly reduced in the
OA+C-A1+HIIT group compared to the OA+C-A1 group (P <
0.01, Figure 6 C-D).