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Fig. 5. Expression of mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinase (JNK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and proinflammatory cytokines in capsaicin-exposed R-DRG-505 cells. Capsaicin treatment induced an increase in the expression levels of p38/JNK MAPK, p65 NF-κB, IL-1β, IL-6, and TNF-α (A) with the concomitant upregulation of autophagy (B), which were reversed by Sec-O-glucosylhamaudol (SOG) treatment. Pharmacological p38/JNK MAPK inhibitors resulted in the consequent inhibition of p65 with decreased expression of proinflammatory cytokines and the downregulation of autophagy. Values were normalized to β-actin levels. The error bars indicate mean ± standard deviation. SB203580: p38 inhibitor, SP600125: JNK inhibitor, IL-1: interleukin-1, IL-6: interleukin-6, TNF-α: tumor necrosis factor-alpha, LC3: microtubule-associated protein 1 light chain 3. aP < 0.05 vs. Capsaicin 0 μM. bP < 0.01 vs. Capsaicin 0 μM. cP < 0.05 vs. Capsaicin 400 μM. dP < 0.01 vs. Capsaicin 400 μM.
Korean J Pain 2021;34:405~416
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