Fortunellin
Fortunellin is a potential anti-inflammation agent in inflammatory diseases, it targets miR-374a, which is a negative regulator of phosphatase and tensin homolog (PTEN). Fortunellin protects against high fructose-induced diabetic heart injury in mice by suppressing inflammation and oxidative stress via AMPK/Nrf-2 pathway regulation.
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Fortunellin protects against high fructose-induced diabetic heart injury in mice by suppressing inflammation and oxidative stress via AMPK/Nrf-2 pathway regulation.[Reference:
WebLink]
Inflammation and oxidative stress contribute to the progression of diabetic cardiomyopathy (DCM).
The study was first designed to calculate the role of an anti-inflammatory and anti-oxidant Fortunellin (For) in high fructose-induced cardiac injury in diabetic mice.
METHODS AND RESULTS:
Fortunellin was found to be none of toxicity to mice and cells using various assays. High fructose was used to induce mice with diabetes. The heart histopathological changes and cardiac function were measured. Fortunellin significantly attenuated the score of histopathological alterations and alleviated heart function, accompanied with reduced inflammation and oxidative stress. The pro-inflammatory cytokines and the expression of p-IκB kinase α (IKKα), p-IκBα, and p-nuclear factor-κB (NF-κB) were dramatically reduced by Fortunellin, while superoxide dismutase (SOD), catalase (CAT), heme oxygenase-1 (HO-1) and p-AMP-activated protein kinase (AMPK) were significantly enhanced. Moreover, in H9C2 cells with nuclear factor erythroid 2-related factor 2 (Nrf2) knock-down abolished the prevention of Fortunellin against cardiac injury, proved by elevated inflammatory response and oxidative stress. Suppression of p-AMPK reduced the level of Nrf2 and HO-1 induced by Fortunellin, eliminating the protective role of Fortunellin.
CONCLUSIONS:
For the first time, our study suggested that Fortunellin protected against fructose-induced inflammation and oxidative stress by enhancing AMPK/Nrf2 pathway in diabetic mice and cardiomyocytes with fructose treatment.
Frontiers in Immunology, 26 Jan 2018, 9:83.
Fortunellin-Induced Modulation of Phosphatase and Tensin Homolog by MicroRNA-374a Decreases Inflammation and Maintains Intestinal Barrier Function in Colitis.[Reference:
WebLink]
Activation of phosphatase and tensin homolog (PTEN) is known to induce cell apoptosis. MicroRNA-374a (miR-374a), which can suppress PTEN expression, has been found abnormally expressed in inflammatory bowel disease (IBD). Fortunellin is a citrus flavonoid that is a potential anti-inflammation agent in inflammatory diseases. The present study investigated the effects and mechanisms underlying Fortunellin-induced inhibition of PTEN in IBD.
METHODS AND RESULTS:
Colitis was established in rats by the intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid to mimic human ulcerative colitis, which is the main type of IBD. miR-374a expression was measured by quantitative real-time polymerase chain reaction, and the regulation of PTEN by miR-374a was evaluated by dual luciferase reporter assay. Western blotting was used to measure the corresponding protein expression. Fortunellin ameliorated colitis symptoms, including excessive inflammation and oxidative stress. Fortunellin decreased epithelial cell apoptosis through inhibiting PTEN expression in colitis. Fortunellin-induced downregulation of PTEN could be counteracted by miR-374a depletion. Moreover, knockdown of miR-374a in vivo partly inhibited the effects of Fortunellin on rat colitis.
CONCLUSIONS:
In conclusion, PTEN inhibition contributes to the amelioration effects of Fortunellin on colitis. It was confirmed that Fortunellin targets miR-374a, which is a negative regulator of PTEN. This study provides novel insights into the pathological mechanisms and treatment alternatives of colitis.
