Multifunctionality of Calebin A in inflammation, chronic diseases and cancer

Abstract

Chronic diseases including cancer have high case numbers as well as mortality rates. The efficient treatment of chronic diseases is a major ongoing medical challenge worldwide, because of their complexity and many inflammatory pathways such as JNK, p38/MAPK, MEK/ERK, JAK/STAT3, PI3K and NF-κB among others being implicated in their pathogenesis. Together with the versatility of chronic disease classical mono-target therapies are often insufficient. Therefore, the anti-inflammatory as well as anti-cancer capacities of polyphenols are currently investigated to complement and improve the effect of classical anti-inflammatory drugs, chemotherapeutic agents or to overcome drug resistance of cancer cells. Currently, research on Calebin A, a polyphenolic component of turmeric (Curcuma longa), is becoming of growing interest with regard to novel treatment strategies and has already been shown health-promoting as well as anti-tumor properties, including anti-oxidative and anti-inflammatory effects, in diverse cancer cells. Within this review, we describe already known anti-inflammatory activities of Calebin A via modulation of NF-κB and its associated signaling pathways, linked with TNF-α, TNF-β and COX-2 and further summarize Calebin A’s tumor-inhibiting properties that are known up to date such as reduction of cancer cell viability, proliferation as well as metastasis. We also shed light on possible future prospects of Calebin A as an anti-cancer agent.

Curcumin Formulations for Better Bioavailability: What We Learned from Clinical Trials Thus Far?

“…Chronic diseases including autoimmune diseases, cancer, cardiovascular diseases, diabetes, hepatocellular, neurological, and renal diseases have persistent high incidence and fatality rates worldwide. , Finding feasible treatment strategies are challenging due to the high prevalence of these diseases and the involvement of several pathways in their development, including JAK/STAT3, JNK, NF-κB, MEK/ERK, p38/MAPK, and PI3K/Akt/mTOR, etc. − Therefore, classical monotarget therapies are insufficient to treat these diseases. Besides, the cost of contemporary pharmaceuticals is high, and have several unfavorable side effects. ,, Indeed, there is an increasing need for the development of safer, effective, multitargeted, and cost-effective therapeutic regimens to replace the current harmful and ineffective treatment approaches.…”

A minor metabolite fromCurcuma longaeffective against metabolic syndrome: results from a randomized, double-blind, placebo-controlled clinical study

“…Hence, it could be a potential compound in managing various human ailments like metabolic disorders, obesity, arthritis, low bone density, and cancer. 16 synthase and activated acetyl-CoA carboxylase. 17 In the animal model of diet induced obesity, Calebin -A supplementation decreased weight gain, and visceral fat accumulation suggested to be mediated by the activation of AMP-activated protein kinase in adipocytes and liver.…”

“…15 Calebin A shows higher chemical stability in acidic and basic media in contrast to the noted instability of curcumin at higher pH values while retaining several physiological properties with curcumin. 16 Calebin A exhibits a variety of pharmacological activities. Hence, it could be a potential compound in managing various human ailments such as metabolic disorders, obesity, arthritis, low bone density, and cancer.…”

“…15 Calebin A shows higher chemical stability in acidic and basic media in contrast to the noted instability of curcumin at higher pH values while retaining several physiological properties with curcumin. 16…”

“…Hence, it could be a potential compound in managing various human ailments such as metabolic disorders, obesity, arthritis, low bone density, and cancer. 16 Lai et al (2015) demonstrated that Calebin A prevents high-fat-diet-induced obesity, inhibits adipocyte differentiation, and ameliorates hepatic steatosis, by suppressing the expression of peroxisome proliferator-activated receptor (PPAR), fatty acid synthase and activated acetyl-CoA carboxylase. 17 In the animal model of diet-induced obesity, Calebin A supplementation decreased weight gain, and visceral fat accumulation, which was suggested to be mediated by the activation of AMP-activated protein kinase in adipocytes and the liver.…”