Amelioration of oxidative stress mediated inflammation and apoptosis in pancreatic islets by Lupeol in STZ-induced hyperglycaemic mice.

BACKGROUND: Type 1 Diabetes mellitus initiates by loss of pancreatic activity which affects other major organs leading to multi-organ failure. Lupeol, a novel phytochemical, is emerging as a potent bioactive molecule. However, the effect of lupeol on hyperglycaemia is not clearly understood. This study delivers an elaborate vision towards the detailed molecular pathway of lupeol against STZ induced diabetic difficulties of the pancreas. METHOD: The current experiments were designed to focus on the ameliorative effect of the triterpene in combating oxidative damage on the pancreas in a preclinical streptozotocin induced mouse model. After diabetic induction, the animals were subjected to administration with 75 mg kg-1 body weight of lupeol, thrice a week for 7 weeks. Histological measurements were done to investigate the anatomy of the pancreas as well as molecular mechanisms were explored. RESULTS: The compound was found to regulate several hyperglycaemic and oxidative stress related markers. Lupeol treatment also reversed the expression levels of inflammatory cytokines (TNF-α and IL-1ß) as well as attenuated the NF-κB mediated inflammatory and extrinsic apoptotic pathway. DISCUSSION: These findings in preclinical streptozotocin induced in vivo mouse model strongly suggest the discovery of novel properties of lupeol against oxidative stress in pancreatic ß cells by regulating the NF-κB and extrinsic apoptotic pathway.

An overview on the role of bioactive α-glucosidase inhibitors in ameliorating diabetic complications.

Recently the use of bioactive α-glucosidase inhibitors for the treatment of diabetes have been proven to be the most efficient remedy for controlling postprandial hyperglycemia and its detrimental physiological complications, especially in type 2 diabetes. The carbohydrate hydrolysing enzyme, α-glucosidase, is generally competitively inhibited by the α-glucosidase inhibitors and results in the delayed glucose absorption in small intestine, ultimately controlling the postprandial hyperglycemia. Here we have reviewed the most recent updates in the bioactive α-glucosidase inhibitors category. This review provides an overview of the α-glucosidase inhibitory potentials and efficiency of controlling postprandial hyperglycemia of various bioactive compounds such as flavonoids, phenolic compound, polysaccharide, betulinic acid, tannins, anthocyanins, steroids, polyol, polyphenols, galangin, procyanidins, hydroxyl-α-sanshool, hydroxyl-ß-sanshool, erythritol, ganomycin, caffeoylquinic acid, resin glycosides, saponins, avicularin, oleanolic acids, urasolic acid, ethanolic extracts etc., from various dietary and non-dietary naturally occurring sources.

The Wnt signaling pathway: a potential therapeutic target against cancer.

The role of the evolutionarily conserved Wnt signaling pathway is well documented in several cellular processes, such as cell proliferation, differentiation, cell motility, and maintenance of the stem cell niche. The very first indication that aberrant Wnt signaling can cause carcinogenesis came from a finding that the mutation of the adenomatous polyposis coli gene (APC) predisposes a person to colorectal carcinoma. Later, with progressing research it became clear that abnormal activation or mutation of the genes related to this pathway could drive tumorigenesis. Here, we review recent advances in research regarding Wnt signaling regulation and its role in several cancer subtypes. Additionally, the utility of Wnt pathway-targeted cancer therapy intervention is also highlighted, with an overview of current approaches to target the Wnt pathway in oncogenesis and the future scopes and challenges associated with them.