University of Calcutta

About: University of Calcutta is a education organization based out in Kolkata, India. It is known for research contribution in the topics: Population & Catalysis. The organization has 8900 authors who have published 19712 publications receiving 259067 citations. The organization is also known as: Calcutta University & CU.

Dinuclear mixed-valence CoIIICoII complexes derived from a macrocyclic ligand: unique example of a CoIIICoII complex showing catecholase activity

Abstract: The work in this paper presents the syntheses, characterization, catecholase activity, and electrospray ionization mass spectroscopic (ESI-MS positive) study of three mixed-valence dinuclear CoIIICoII complexes of composition [CoIIICoIIL(N3)3]·CH3CN (1), [CoIIICoIIL(OCN)3]·CH3CN (2), and [CoIIICoIIL(μ-CH3COO)2](ClO4) (3), derived from a tetraimino diphenolate macrocyclic ligand H2L, obtained on [2 + 2] condensation of 4-ethyl-2,6-diformylphenol and 2,2′-dimethyl-1,3-diaminopropane. While 1 and 2 are diphenoxo-bridged, 3 is a heterobridged bis(μ-phenoxo)bis(μ-acetate) system. Utilizing 3,5-di-tert-butyl catechol (3,5-DTBCH2) as the substrate, the catecholase activity of all the three complexes has been checked in methanol/acetonitrile/N,N-dimethyl formamide. While 2 and 3 are inactive, complex 1 shows catecholase activity with turnover numbers of 482.16 h−1 and 45.38 h−1 in acetonitrile and methanol, respectively. Electrospray ionization mass (ESI-MS positive) spectra of complexes 1–3 have been recorded in acetonitrile solutions and the positive ions have been well characterized. The ESI-MS positive spectrum of complex 1 in the presence of 3,5-DTBCH2 has also been recorded and, interestingly, two positive ions [CoIIICoIIL(N3)2(3,5-DTBCH−)H]+ and [CoIICoIIL(μ-3,5-DTBCH2−)Na]+ have been identified.

Protocatechuic acid, a phenolic from sansevieria roxburghiana leaves, suppresses diabetic cardiomyopathy via stimulating glucose metabolism, ameliorating oxidative stress, and inhibiting inflammation

Abstract: Persistent hyperglycemia, impairment of redox status and establishment of inflammatory pathophysiology integrally play important role in the pathogenesis of diabetic cardiomyopathy (DC). Present study examined the therapeutic potential of protocatechuic acid isolated from the Sansevieria roxburghiana rhizomes against DC employing rodent model of type 2 diabetes (T2D). T2D was induced by high fat diet + a low-single dose of streptozotocin, (35 mg/kg, i.p.). T2D rats exhibited significantly (p < 0.01) high fasting blood glucose level. Alteration in serum lipid profile (p < 0.01) and increased levels of lactate dehydrogenase (p < 0.01) and creatine kinase (p < 0.01) in the sera of T2D rats revealed the occurrence of hyperlipidemia and diabetic pathophysiology. A significantly (p < 0.01) high levels of serum C-reactive protein and pro-inflammatory mediators revealed the establishment of inflammatory occurrence in T2D rats. Besides, significantly high levels of troponins in the sera revealed the establishment of cardiac dysfunction in T2D rats. However, protocatechuic acid (50 and 100 mg/kg, p.o.) treatment could significantly reverse the changes in serum biochemical parameters related to cardiac dysfunctions. Molecular mechanism studies demonstrated impairment of signaling cascade, IRS1/PI3K/Akt/AMPK/p 38/GLUT4, in glucose metabolism in the skeletal muscle of T2D rats. Significant (p < 0.01) activation of polyol pathway, enhanced production of AGEs, oxidative stress and up-regulation of inflammatory signaling cascades (PKC/NF-κB/PARP) were observed in the myocardial tissue of T2D rats. However, protocatechuic acid (50 and 100 mg/kg, p.o.) treatment could significantly (p < 0.05-0.01) stimulate glucose metabolism in skeletal muscle, regulated glycemic and lipid status, reduced the secretion of pro-inflammatory cytokines, and restored the myocardial physiology in T2D rats near to normalcy. Histological assessments were also in agreement with the above findings. In silico molecular docking study again supported the interactions of protocatechuic acid with different signaling molecules, PI3K, IRS, Akt, AMPK PKC, NF-κB and PARP, involved in glucose utilization and inflammatory pathophysiology. In silico ADME study predicted that protocatechuic acid would support the drug-likeness character. Combining all, results would suggest a possibility of protocatechuic acid to be a new therapeutic agent for DC in future.

Inflammation-induced ROS generation causes pancreatic cell death through modulation of Nrf2/NF-κB and SAPK/JNK pathway.

Abstract: Chronic pancreatitis is characterized by progressive loss of exocrine and endocrine functions of the pancreas and is considered to be the single most important cause for development of pancreatic cancer. Recent evidence suggests that inflammation and oxidative stress play pivotal roles in the development of clinical conditions like pancreatitis, type 2 diabetes mellitus, and metabolic syndrome. Nonetheless, molecular signaling pathways linking inflammation, oxidative stress, and pancreatic cell death are not yet well defined. In this study, bacterial lipopolysaccharide (LPS) was used (injected twice a week for three weeks) to emulate a chronic systemic inflammatory state in experimental Swiss albino mice. Using this model, we traced the genesis of inflammation-induced pancreatic dysfunction and mapped the signaling events which contribute to the induction of this state. Histopathological studies revealed the appearance of cell injuries and increased collagen content in LPS-exposed group, indicative of fibrosis. Assays for intraperitoneal glucose tolerance, insulin levels, and insulin receptor mRNA expression signified inflammation-induced insulin insensitivity. For the first time we present evidence that cellular inflammation and subsequent oxidative stress modulate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/NF-E2-related factor 2 or Nuclear factor (erythroid-derived 2)-like 2 pathway and initiates pancreatic cell death by activation of stress-responsive Rho/stress-activated protein kinase or SAPK/Jun-N-terminal kinase (JNK) pathway. Scavenging of intracellular reactive oxygen species (ROS) by a standard antioxidant N-acetyl cysteine led to pancreatic cell survival. The data obtained strongly indicates that the LPS/toll-like receptor-4 or TLR-4/ROS/NF-κB pathway is critically involved in the initiation of inflammation, oxidative stress, and pancreatic cell death and might prove to be an excellent choice as a target for novel therapeutic strategies in the management of metabolic disorders.

Effect of lead and arsenic on murine macrophage response

Abstract: Splenic macrophages are highly efficient in trapping and concentrating foreign substances carried in the blood and also the major sites where antibodies are synthesised and from where they are released into the circulation. Lead and Arsenic as environmental agents are considered to be high priority toxic substances largely due to their carcinogenic potentials in humans. However, these heavy metals as carcinogens remain an enigma because while they are definitely active in humans, carcinogenesis in the rodent model has never been convincingly demonstrated. Although macrophages are predominantly recruited to the site of inflammation during inflammatory distress as well as in immune response, nothing is known about the interaction of lead and arsenic with macrophages and their possible role in immunotoxicologic effect. In the present study it is reported that in vivo lead acetate treatment (10 mg/kg body wt) inhibits the cell adhesion property and alters the cell morphology in the splenic macrophages...