Coenzyme Q10 Inhibits Th17 and STAT3 Signaling Pathways to Ameliorate Colitis in Mice

Abstract

Coenzyme Q10 (CoQ10) is a powerful antioxidant substance synthesized in the body. The current study aimed to determine whether CoQ10 suppresses inflammation and inhibits p-STAT3 expression in an experimental colitis mouse model. The mice were orally fed with CoQ10 once a day for 13 days. Histological analysis of the colons was performed by immunohistochemistry. Expression of IL-17, FOXP3, p53, AMPK, and mTOR and activation of p-STAT3 and p-STAT5 in lymph node and spleen tissues were detected by confocal microscopy of stained tissue sections. The relative mRNA expression was measured with real-time PCR, and protein levels were examined by western blot. CoQ10 reduced the disease activity index score and the colon histological score. It also reduced inflammatory mediators in the colon and increased the colon length. The expression of IL-17 and p-STAT3 was decreased with CoQ10 treatment. In contrast, CoQ10 treatment increased the expression of p-AMPK and FOXP3. Expression of anti-inflammatory cytokines was shown to increase in colitis mice treated with CoQ10. These results suggested that CoQ10 may reduce the severity of colitis and suppress inflammation through the inhibition of p-STAT3 and IL-17. These results support the use of CoQ10 as a potential targeted therapy for the treatment of colitis.

miR‑146a regulates the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF‑κB signaling by targeting TRAF6

“…Activation of the STAT signaling pathway determines the differentiation direction of T cells. Thus, it regulates a series of physiological and pathological processes (18). Of them, the STAT3 protein has been indicated to play a critical role in regulating Th17 cell differentiation (18).…”

“…Thus, it regulates a series of physiological and pathological processes (18). Of them, the STAT3 protein has been indicated to play a critical role in regulating Th17 cell differentiation (18). Abnormalities in the STAT3 signaling pathway is related to the genesis of multiple diseases, such as infections, tumors and autoimmune diseases (19,20).…”

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

“…Our previous studies showed that CoQ10 inhibited autoimmune disease pathogenesis [15,16]. We also demonstrated that CoQ10 suppresses Th17 cells in experimental autoimmune arthritis mice via inhibition of the signal transducer and activator of transcription (STAT3) signaling pathway [17,18].…”

“…In our previous studies, we demonstrated that CoQ10 has anti-inflammatory functions through the suppression of Th17 cells [15][16][17]. In particular, we showed that CoQ10 inhibited Th17 cells through the suppression of phosphorylated STAT3 (p-STAT3) production [18]; p-STAT3 is the activated form of STAT3, and is known to increase levels of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β [26].…”

miR-135a Protects Dextran Sodium Sulfate-Induced Inflammation in Human Colorectal Cell Lines by Activating STAT3 Signal

“…Thus, targeting cytokines balance has resulted in the development of multiple biological agents in IBD. Also, cytokine-mediated activation of signal transducers and activators of transcription factor (STAT) 3 in the epithelial lining cells has been reported to improve cellular protection, survival, and proliferation in IBD models, including dextran sodium sulfate (DSS) colitis model [9][10][11]. Compared with other chemicals-induced experimental models, DSS serves as a direct chemical toxin to colonic epithelium leading to epithelial cell injury and the DSS model has been widely used in IBD research due to its rapidity, simplicity, reproducibility and controllability [12].…”