Domonkos Feher - Momordica charantia (bitter melon) attenuates high-fat diet-associated oxidative stress and neuroinflammation.

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  Nerurkar,   Pratibha V.; Johns, Lisa M.; Buesa, Lance M.; Kipyakwai, Gideon;   Volper, Esther; Sato, Ryuei; Shah, Pranjal; Fehér, Domonkos;   Williams, Philip G.; Nerurkar, Vivek R. Journal of Neuroinflammation  2011,   8, 64.



  The   rising epidemic of obesity is associated with cognitive decline   and is considered as one of the major risk factors for   neurodegenerative diseases. Neuroinflammation is a critical   component in the progression of several neurological and   neurodegenerative diseases. Increased metabolic flux to the brain   during overnutrition and obesity can orchestrate stress response,   blood-brain barrier (BBB) disruption, recruitment of inflammatory   immune cells from peripheral blood and microglial cells   activation leading to neuroinflammation. The lack of an effective   treatment for obesity-associated brain dysfunction may have   far-reaching public health ramifications, urgently necessitating   the identification of appropriate preventive and therapeutic   strategies. The objective of our study was to investigate the   neuroprotective effects of Momordica charantia (bitter melon) on   high-fat diet (HFD)-associated BBB disruption, stress and   neuroinflammatory cytokines. C57BL/6 female mice were fed HFD   with and without bitter melon (BM) for 16 weeks. BBB disruption   was analyzed using Evans blue dye. Phosphate-buffered saline   (PBS) perfused brains were analyzed for neuroinflammatory markers   such as interleukin-22 (IL-22), IL-17R, IL-16, NF-κB1, and glial   cells activation markers such as Iba1, CD11b, GFAP and S100β.   Additionally, antioxidant enzymes, ER-stress proteins, and   stress-resistant transcription factors, sirtuin 1 (Sirt1) and   forkhead box class O transcription factor (FoxO) were analyzed   using microarray, quantitative real-time RT-PCR, western   immunoblotting and enzymatic assays. Systemic inflammation was   analyzed using cytokine antibody array. BM ameliorated   HFD-associated changes in BBB permeability as evident by reduced   leakage of Evans blue dye. HFD-induced glial cells activation and   expression of neuroinflammatory markers such as NF-κB1, IL-16,   IL-22 as well as IL-17R were normalized in the brains of mice   supplemented with BM. Similarly, HFD-induced brain oxidative   stress was significantly reduced by BM supplementation with a   concomitant reduction in FoxO, normalization of Sirt1 protein   expression and up-regulation of Sirt3 mRNA expression.   Furthermore, plasma antioxidant enzymes and pro-inflammatory   cytokines were also normalized in mice fed HFD with BM as   compared to HFD-fed mice. Functional foods such as BM offer a   unique therapeutic strategy to improve obesity-associated   peripheral inflammation and neuroinflammation.

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