Nicotine sensing behavior of nickel(II) complexes catalyzed oxidation and coupling reactions.

One of the main source of demise during the next ten years will be coronary heart disease and stroke, which are brought on by smoking (nicotine). To identify the percentage (%) of nicotine consumption by electrocatalytic sensor towards nicotine for target-specific prevent stroke, four uninuclear Ni2+ complexes of substituted butanimidamide Schiff base ligands [H2L1-4] was prepared. All the complexes were thoroughly analyzed by using several spectroscopic techniques such as CHNS analysis, FT-IR, NMR (1H & 13C) UV-Vis and NMR. The analyses showed tetradentate binding mode of ligand around nickel(II) metal ion leads to the structure of square planar with N2X2 (X = O, S) donor fashion. In addition, the well-defined nickel(II) complexes were utilized for oxidation of various alcohols such as cyclohexanol, and benzyl alcohol were produced to the assorted oxidized products with high yield respectively using greener co-oxidant (molecular oxygen). In addition, Nickel(II) complexes was further utilized as catalyst for aryl-aryl coupling reaction via Suzuki-Mayura method to obtain biphenyl compound. Furthermore, nickel(II) complexes were exploited for electrochemical detection of nicotine sensing in µM concentration.

Moringa concanensis Nimmo extracts ameliorates hyperglycemia-mediated oxidative stress and upregulates PPARγ and GLUT4 gene expression in liver and pancreas of streptozotocin-nicotinamide induced diabetic rats.

The current study investigates the effects of ethanolic extract of M. concanensis Nimmo leaves (EEMCNL) with respect to its potent protective tissue damage, antioxidant properties in serum, liver and kidney, histopathological evaluation, and PPARγ and GLUT4 gene expression in liver and pancreatic tissue of Streptozotocin-Nicotinamide (STZ-NA) induced diabetic rats. Animals were divided into five groups (n = 5): control; diabetic; diabetic + EEMCNL; control + EEMCNL; and diabetic + glibenclamide. After 45 days of treatment with EEMCNL, MDA levels were significantly decreased in the diabetic-induced group when compared with the STZ-induced diabetic group (P < 0.05). The activities of serum enzymes AST, ALT, ALP, ACP and LDH were significantly decreased in serum and kidney, and increased in liver tissues of the EEMCNL-treated group as compared with the STZ-NA induced diabetic group (P < 0.05). The levels of total protein, urea, creatinine and uric acid observed in the diabetic group returned to normal by administration of EEMCNL (250 mg/kg) as relative to the STZ-NA induced diabetic group (P < 0.05). Furthermore, EEMCNL upregulated PPARγ and GLUT4 expression in liver and pancreatic tissue of the STZ-NA induced diabetic group rats. Taken together, these findings contribute to a better understanding of the hepatoprotective and renoprotective potential of EEMCNL against oxidative stress in the diabetic state, which was evidenced by the capacity of EEMCNL to modulate the antioxidant defence and to decrease lipid peroxidation in these tissues.

Moringa concanensis Nimmo ameliorates hyperglycemia in 3T3-L1 adipocytes by upregulating PPAR-γ, C/EBP-α via Akt signaling pathway and STZ-induced diabetic rats.

Moringa concanensis Nimmo is a medicinal plant for treating various human illnesses including menstrual pain, high blood pressure, jaundice, inflammation, pain, fever, sore eyes, and cholesterol in Indian folk medicine. Despite its versatility, its antihyperglycemic mechanism of action (in vitro and in vivo) remains unclear. Therefore, in this study we developed the possible antihyperglycemic mechanism of action in 3T3-L1 cells by evaluating mRNA and protein expression, which are associated with adipogenesis and lipogenesis (insulin sensitizer). Also, the antihyperglycemic activity of the ethanolic extract of M. concanensis Nimmo leaves (EEMCN) was evaluated on glucose, insulin, biochemical, and lipid profile in experimental diabetic rat models induced with streptozotocin (STZ). Results showed that EEMCN leaves enhanced lipid accumulation in 3T3-L1 cells, as assessed by Oil Red O staining, and upregulated gene expression level of PPAR-γ, C/EBP-α, t-SREBP, FAS, Glut-4, adipogenin, DAG, and LPL through Akt signaling in 3T3-L1 cells. Also, EEMCN treatment increased body weight and insulin level and lowered blood glucose, HbA1c, amylase, and lipid profile level in STZ-induced diabetic rats. In conclusion, EEMCN possesses in vivo antidiabetic potential, having such efficacy through a mechanism of action that involves antihyperglycemic, hypoglycemic, and potential insulin sensitizer (PPAR-γ, C/EBP-α/Akt over expression) action.