Plant Compounds for the Treatment of Diabetes, a Metabolic Disorder: NF-κB as a Therapeutic Target

• Published in: Current pharmaceutical design Vol. 26; no. 39; p. 4955
• Main Authors: Sahukari, Ravi, Punabaka, Jyothi, Bhasha, Shanmugam, Ganjikunta, Venkata S, Ramudu, Shanmugam K, Kesireddy, Sathyavelu R
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2020
• Subjects: Animals; Diabetes Complications; Diabetes Mellitus, Experimental; Humans; Inflammation - drug therapy; NF-kappa B - metabolism; Oxidative Stress; diabetic complications; inflammatory mediators; NF-κB; hyperglycemia; natural products; Diabetes; insulin resistance
• ISSN: 1873-4286
• DOI: 10.2174/1381612826666200730221035

The prevalence of diabetes in the world population hás reached 8.8 % and is expected to rise to 10.4% by 2040. Hence, there is an urgent need for the discovery of drugs against therapeutic targets to sojourn its prevalence. Previous studies proved that NF-κB serves as a central agent in the development of diabetic complications. This review intended to list the natural plant compounds that would act as inhibitors of NF-κB signalling in different organs under the diabetic condition with their possible mechanism of action. Information on NF-κB, diabetes, natural products, and relation in between them, was gathered from scientific literature databases such as Pubmed, Medline, Google scholar, Science Direct, Springer, Wiley online library. NF-κB plays a crucial role in the development of diabetic complications because of its link in the expression of genes that are responsible for organs damage such as kidney, brain, eye, liver, heart, muscle, endothelium, adipose tissue and pancreas by inflammation, apoptosis and oxidative stress. Activation of PPAR-α, SIRT3/1, and FXR through many cascades by plant compounds such as terpenoids, iridoids, flavonoids, alkaloids, phenols, tannins, carbohydrates, and phytocannabinoids recovers diabetic complications. These compounds also exhibit the prevention of NF-κB translocation into the nucleus by inhibiting NF-κB activators, such as VEGFR, RAGE and TLR4 receptors, which in turn, prevent the activation of many genes involved in tissue damage. Current knowledge on the treatment of diabetes by targeting NF-κB is limited, so future studies would enlighten accordingly.