Online ISSN: 2515-8260

Keywords : 1


Antioxidant Activity Of Some Triazoles Synthesized By Click Chemistry

Jalal Hasan Mohammed; Saadon Abdulla Aowda

European Journal of Molecular & Clinical Medicine, 2020, Volume 7, Issue 8, Pages 688-704

In this research, eight new compounds were created from the interaction of a number of aromatic and aliphatic compounds with propargyl bromide to prepare the alkynes after that; alkynes is reacted with the organic azide to form eight new compounds of 1,2,3-triazole by click reaction Using copper as a catalyst After that an antioxidant was done For prepared triazole , DPPH radical scavenging activity and It was the best result values 76.54+-1.9 for compound 9 Compared to the standard model ascorbic acid values 86.03+-4.02 at 200 mg/ml concentration

A Convenient Synthesis and Reactions ofsome Substituted 1,2,4-Triazine, and Their Derivatives with Carbazole, Sulfonamide and Trityl Chloride Moiety of Biological Interest

Aarfah Majid; Mohammad Ashid; Nasir Hussain; AjitJoshi .

European Journal of Molecular & Clinical Medicine, 2020, Volume 7, Issue 8, Pages 994-1002

A series of 1,2,4-triazine derivatives [1-9] were synthesized by various analogous methods. In this investigation 5,6-diphenyl-1,2,4-triazine-3-thiol compound [1] was prepared by cyclization of benzil with thiosemicarbazide. Further 5-(prop-2-en-1-yl)-5H-[1,2,4] triazino [5,6-b]indole-3-thiol compound [3] was prepared by treating 1-(prop-2-en-1-yl)-1h-indole-2,3-dione compound [2] with thiosemicarbazide. Further a variety of compounds were prepared by hydrogen replacement of compound [1] and compound [3] by differently active halogen containing scaffolds. Compound [1] was reacted with 9-(2-bromoethyl)-9H-carbazole to produce 9-(2-(5,6-diphenyl-1,2,4-triazin-3-yl)thio)ethyl)9-H-carbazole compound [4].After that, the compound [1] was allowed to react with 2-chloro-N-(4-methylbenzene-1-sulfonyl)-N-(pyridine-2-yl) acetamide to synthesize 2-((5,6-diphenyl-1,2,4-triazin-3-yl)-N-(Pyridin-2-yl)-N-tosylacetamide compound [5].In addition to this ,5,6-diphenyl-3-(tritylthio)-1,2,4-triazine compound [6] was also prepared by condensation reaction between trityl chloride and compound [1]. Further, Compound [3] was reacted with 9-(2-bromoethyl)-9H-carbazole to produce 3-((2-(9H-Carbazol-9-yl)ethylthio)-5-allyl-5H-[1,2,4]triazino[5,6-b]triazino[5,6-b]indole compound [7].After that, the compound [3] was allowed to react with 2-chloro-N-(4-methylbenzene-1-sulfonyl)-N-(pyridine-2-yl) acetamide to synthesize 2-((5-allyl-5H-[1,2,4]triazino[5,6-b]infol-3-yl)thio)-N-(pyridine-2-yl)-N-tosylacetamide compound [8].In addition to this ,5-allyl-3-(tritylthio)-5H-[1,2,4]triazino compound [9] was also prepared by condensation reaction between trityl chloride and compound [3]. All the synthesized compounds were confirmed by spectral data (Table 1) and analytical data (Table 2).

SYNTHESIS OF REMARKABLE SUBSTITUTED ARYL 1,3,4-OXADIAZOLE DERIVATIVES AND THEIR POTENT ANTIINFLAMMATORY AND ANALGESIC ACTIVITIES

Vishal kumar; Satish Kumar Sharma; Rizwan Ahmad

European Journal of Molecular & Clinical Medicine, 2020, Volume 7, Issue 1, Pages 4406-4415

The key objective of the current research is to synthesize and analgesic action 5- (2-(2,3-dimethylphenylamino)phenyl)-2-(aryl)- 1,3,4-oxadiazole and to test this activity (VT1- VT8). During this investigation, the condensed methanone {2-[(2,3- dimethylphenyl)amino]phenyl}(hydrazinyloxide), and various aryl-acids in presence of phosphorous oxychloride were synthesized in the present investigations by a sequence of 5-(2- (2,3-dimethylphenylamino)phenyl]-2,3,4-oxadiazols (VT1-VT8). Both synthesized compounds have been tested with 50 mg/kg and 10 mg/kg po respectively for their in vivo antiinflammatory and analgesic activities. Carrageen's mediated acute rat paw oedema model and Eddy's hot plate system were used to analyze the anti-inflammatory and analgesic function of the synthesized compounds. Any substances have been effective at their anti-inflammatory and analgesic activities, according to biological results. Elemental research (C, H, N) and spectral analysis also verified the composition of both substances (IR, 1H NMR and mass spectrometry).

Regulation of renal fibrosis by the transforming growth factor beta-1 receptor Alk1

Carlos Martínez-Salgado; Carlos Martínez-Salgado; Carlos Martínez-Salgado; Carlos Martínez-Salgado; Jose M. Muñoz-Felix; Jose M. Muñoz-Felix; Jose M. Muñoz-Felix; Jose M. Muñoz-Felix; Nuria Perretta-Tejedor

European Journal of Molecular & Clinical Medicine, 2015, Volume 2, Issue 2, Pages -

Tubulointerstitial fibrosis –a common end-stage feature of chronic kidney disease- is characterized by the presence of renal myofibroblasts and excessive accumulation of extracellular matrix proteins (ECM) in the renal tubular interstitium. The cytokine transforming growth factor beta 1 (TGF-β1) promotes myofibroblast activation and ECM proteins expression through intracellular Smads activation, having an important role in renal fibrosis. We have recently reported that the heterozygous disruption of the TGF-β1 receptor activin receptor-like kinase 1 (ALK1) leads to an increase in TGF-β induced renal fibrosis after ureteral obstruction. Thus, we analyzed the effect of ALK1 heterozygosity in TGF-β1 induced signaling and its consequent fibrotic response in mouse embryonic fibroblasts (MEFs). We have analyzed Smad signaling pathaways in ALK1 heterozygous MEFs (ALK1+/-) and their respective controls (ALK1+/+) in basal conditions and after TGF-β1 treatment by Western blot and immunofluorescence. Moreover, we have analyzed collagen I, fibronectin and connective tissue growth factor (CTGF) expression in basal conditions, after TGF-β1 stimulation and after ALK5 inhibition –with SB431542- and Smad3 inhibition –with SIS3-. TGF-β1 stimulation induced Smad2 and Smad3 phosphorylation and Smad2/3 translocation into the nucleus in ALK1+/+ and ALK1+/- MEFs, being this increase higher in ALK1+/- MEFs. Basal Smad2 and Smad3 phosphorylation was higher in ALK1 heterozygous fibroblasts. TGF-β1 stimulation did not induce Smad1 phosphorylation in ALK1+/- MEFs and a very small Smad1 phosphorylation in ALK1+/- MEFs. ALK1 heterozygous MEFs expressed more collagen I, fibronectin and CTGF than their respective controls in basal conditions. Stimulation with TGF-β1 lead to an increase in collagen I, fibronectin and CTGF, being the increase in fibronectin and CTGF higher in ALK1+/- MEFs. Inhibition of ALK5 and Smad3 reversed the ALK1+/- phenotype.