01672nas a2200265 4500008004100000022001400041245010700055210006900162260007500231300001000306490000600316520072300322653001701045653002101062653002701083653001601110100001601126700002101142700002501163700002501188700002301213700002601236700002001262856012401282 2012 eng d a1862-834600aDynamic proteome in enigmatic preeclampsia: an account of molecular mechanisms and biomarker discovery0 aDynamic proteome in enigmatic preeclampsia an account of molecul aPOSTFACH 101161, 69451 WEINHEIM, GERMANYbWILEY-V C H VERLAG GMBHcJAN a79-900 v63 a

The coevolution of genomics and proteomics has led to advancements in the field of diagnosis and molecular mechanisms of disease. Proteomics is now stepping into the field of obstetrics, where early diagnosis of pregnancy complication such as preeclampsia (PE) is imperative. PE is a multifactorial disease characterized by hypertension with proteinuria, which is a leading cause of maternal and neonatal morbidity and mortality occurring in 5-7% of pregnancies worldwide. This review discusses the probable molecular mechanisms that lead to PE and summarizes the proteomics research carried out in understanding the pathogenicity of PE, and for identifying the candidate biomarker for diagnosis of the disease.

10aHypertension10aOxidative stress10aPregnancy complication10aProteinuria1 aMary, Sheon1 aPatil, Gouri, V.1 aKulkarni, Asmita, V.1 aKulkarni, Mahesh, J.1 aJoshi, Sadhana, R.1 aMehendale, Savita, S.1 aGiri, Ashok, P. uhttps://library.ncl.res.in/content/dynamic-proteome-enigmatic-preeclampsia-account-molecular-mechanisms-and-biomarker-002789nas a2200289 4500008004100000022001400041245015800055210006900213260000800282300001400290490000700304520175600311653002102067653001702088653003302105653002102138653002002159100002502179700002102204700003202225700002202257700002002279700002502299700002202324700002402346856012902370 2020 eng d a0721-759500aEnzymatic and non-enzymatic detoxification of reactive carbonyl compounds improves the oxidative stress tolerance in cucumber, tobacco and rice seedlings0 aEnzymatic and nonenzymatic detoxification of reactive carbonyl c cSEP a1359-13720 v393 a

Detoxification of reactive carbonyl compounds (RCC) is crucial to sustain cellular activity to improve plant growth and development. Seedling growth is highly affected by accumulation of RCC under stress. We report non-enzymatic, enzymatic mechanisms of detoxification of RCC in the cucumber, tobacco and rice seedling systems exposed to glucose, NaCl, methyl viologen (MV) induced oxidative stress. The cucumber seedlings exposed to carbonyl stress had higher levels of malondialdehyde (MDA), protein carbonyls (PCs) and advanced glycation end-product N-carboxymethyl-lysine (AGE-CML) that negatively affected the seedling growth. The overexpression of enzyme encoding aldo-keto reductase-1 (AKR1) in tobacco and rice showed detoxification of RCC, MDA and methylglyoxal (MG) with improved seedling growth under glucose, NaCl and MV-induced oxidative stress. Further, small molecules like acetylsalicylic acid (ASA), aminoguanidine (AG), carnosine (Car), curcumin (Cur) and pyridoxamine (PM) showed detoxification of RCC non-enzymatically and rescued the cucumber seedling growth from glucose, NaCl and MV-stress. In autotrophically grown rice seedlings these molecules substantially improved seedling growth under MV-induced oxidative stress. Seedlings treated with the small molecules sustained higher guaiacol peroxidase (GPX) enzyme activity signifying the role of small molecules in reducing carbonyl stress-induced protein inactivation and AGE-CML protein modifications. The results showed that besides enzymatic detoxification of RCC, the small molecules also could reduce cytotoxic effect of RCC under stress. The study demonstrates that small molecules are attractive compounds to improve the seedling growth under stress conditions.

10aOxidative stress10aplant growth10aReactive carbonyl scavengers10aSeed germination10asmall molecules1 aNareshkumar, Ambekar1 aSubbarao, Sindhu1 aVennapusa, Amarnatha, Reddy1 aAshwin, Vargheese1 aBanarjee, Reema1 aKulkarni, Mahesh, J.1 aRamu, Vemanna, S.1 aUdayakumar, Makarla uhttps://library.ncl.res.in/content/enzymatic-and-non-enzymatic-detoxification-reactive-carbonyl-compounds-improves-oxidative02781nas a2200313 4500008004100000022001400041245018000055210006900235260000900304300001100313490000900324520172200333653002402055653001902079653000902098653001102107653002102118653001802139100002102157700002102178700001602199700002702215700002402242700001002266700002502276700001902301700001902320856012802339 2021 eng d a0006-899300aProtriptyline improves spatial memory and reduces oxidative damage by regulating NF kappa B-BDNF/CREB signaling axis in streptozotocin-induced rat model of Alzheimer's disease0 aProtriptyline improves spatial memory and reduces oxidative dama cMAR  a1472610 v17543 a

Antidepressants are well known to exert their role via upregulation of brain derived neurotrophic factor (BDNF). BDNF has been reported to exerts its neuroprotective effect in rodent and primate models as well as in patients of Alzheimer's disease (AD). The aim of our study was to evaluate the effect of protriptyline (PRT), a tricyclic antidepressant, in streptozotocin (STZ)- induced rat model of AD. Total 10 mu l of STZ was injected into each ventricle (1 mg/kg). PRT (10 mg/kg, i.p.) treatment was started 3-day post STZ administration and continued till 21 days. We found that STZ treatment significantly increased pTau, A beta 42 and BACE-1 expression, oxidative stress and neurodegeneration in hippocampus and cortex of adult rats. STZ induced impairment in spatial learning and retention memory was associated with increased WO and reduced CREB and BDNF expression in cortex and hippocampus. Interestingly, PRT treatment significantly reduced pTau, A beta 42 and BACE-1 levels, neurodegeneration, oxidative stress and glial activation, contributing to the improved spatial learning and retention memory in STZ treated rats. Moreover, PRT treatment significantly improved p-ERK/ERK ratio and enhanced BDNF and CREB levels by reducing NFXB and GFAP expression in STZ treated rats. Our data suggest that impaired NFXB and CREB signaling potentially contribute in AD pathogenesis by elevating oxidative stress and neuroinflammation mediated neurodegeneration. Our study has established protriptyline as a multi target molecule in pre-clinical model of AD and further investigations on PRT like molecules could pave way for further development of effective new treatments in neurodegenerative disorders.

10aAlzheimer's disease10aantidepressant10aBDNF10aMemory10aOxidative stress10aProtriptyline1 aTiwari, Virendra1 aMishra, Akanksha1 aSingh, Sonu1 aMishra, Sandeep, Kumar1 aSahu, Kiran, Kumari1 aParul1 aKulkarni, Mahesh, J.1 aShukla, Rakesh1 aShukla, Shubha uhttps://library.ncl.res.in/content/protriptyline-improves-spatial-memory-and-reduces-oxidative-damage-regulating-nf-kappa-b02430nas a2200277 4500008004100000022001400041245014100055210006900196260000800265300001100273490000800284520148100292653001501773653001301788653001801801653003301819653002101852653001501873100002501888700001901913700002401932700002301956700002501979700002102004856012702025 2024 eng d a0278-691500aSWATH-MS reveals that bisphenol A and its analogs regulate pathways leading to disruption in insulin signaling and fatty acid metabolism0 aSWATHMS reveals that bisphenol A and its analogs regulate pathwa cJUN a1146670 v1883 a

Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC), associated with obesity and insulin resistance. The FDA prohibited the use of BPA-based polycarbonate resins in infant formula packaging; thus, its analogs, viz. Bisphenol S (BPS) and Bisphenol F (BPF) were considered alternatives in epoxy resins, plastics, and food cans. As these analogs might evoke a similar response, we investigated the role of Bisphenols (BPA, BPF, and BPS), on insulin signaling in CHO-HIRc-myc-GLUT4eGFP cells at environmentally relevant concentrations of 2 nM and 200 nM. Insulin signaling demonstrated that Bisphenols reduced phosphorylation of IR and AKT2, GLUT4 translocation, and glucose uptake. This was accompanied by increased oxidative stress. Furthermore, SWATHMS-based proteomics of 3T3-L1 cells demonstrated that Bisphenol-treated cells regulate proteins in insulin resistance, adipogenesis, and fatty acid metabolism pathways differently. All three Bisphenols induced differentially expressed proteins enriched similar pathways, although their abundance differed for each Bisphenol. This might be due to their varying toxicity level, structural differences, and estrogen-mimetic activity. This study has important implications in addressing health concerns related to EDCs. Given that the analogs of BPA are considered alternatives to BPA, the findings of this study suggest they are equally potent in altering fatty acid metabolism and inducing insulin resistance.

10aBisphenols10aEstrogen10aLipid droplet10aMitochondrial beta-oxidation10aOxidative stress10aPPAR gamma1 aKulsange, Shabda, E.1 aSharma, Monika1 aSonawane, Babasaheb1 aJaiswal, Meera, R.1 aKulkarni, Mahesh, J.1 aSanthakumari, B. uhttps://library.ncl.res.in/content/swath-ms-reveals-bisphenol-and-its-analogs-regulate-pathways-leading-disruption-insulin