82575-82-4Relevant articles and documents
TRYPTAMINE DERIVATIVES, THEIR PREPARATION AND THEIR USE IN GASTROPATHY
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Paragraph 0101; 0107; 0108; 0119, (2013/08/14)
The synthesis and evaluation of gastroprotective effect of different tryptamine derivatives. Tryptamine derivatives have been synthesized by formation of amide or ester with some known anti oxidant molecules. These derivatives show excellent antioxidant property in vitro. Among all the derivatives the compound SEGA (3a), that was prepared by the combination of serotonin with gallic acid shows the greater antioxidant property than the other synthesized compounds both in vivo and in vitro. SEGA(3a) shows the gastroprotective effect against NSAIDs (indomethacin or diclofenac)-induced gastropathy in dose dependent manner and also accelerates the healing from injury. It prevents the NSAIDs-induced mitochondrial oxidative stress in vivo. This derivative prevents NSAID-induced mitochondrial oxidative stress-mediated apoptosis in vivo by preventing the activation of caspase 9 and caspase-3 and restores NSAIDs-mediated collapse of mitochondroial transmembrane potential and dehydrogenase activity. SEGA (3a) plays an important role as an iron chelator as well as intra mitochondrial ROS scavenger. Thus, SEGA (3a) is a potent antioxidant antiapototic molecule, which efficiently prevents NSAID-induced gastropathy and stress or alcohol-mediated gastric damage.
Tryptamine-gallic acid hybrid prevents non-steroidal anti-inflammatory drug-induced gastropathy: Correction of mitochondrial dysfunction and inhibition of apoptosis in gastric mucosal cells
Pal, Chinmay,Bindu, Samik,Dey, Sumanta,Alam, Athar,Goyal, Manish,Iqbal, Mohd Shameel,Sarkar, Souvik,Kumar, Rahul,Halder, Kamal Krishna,Debnath, Mita Chatterjee,Adhikari, Susanta,Bandyopadhyay, Uday
experimental part, p. 3495 - 3509 (2012/06/15)
We have investigated the gastroprotective effect of SEGA(3a), a newly synthesized tryptamine-gallic acid hybrid molecule against non-steroidal anti-inflammatory drug (NSAID)-induced gastropathy with mechanistic details. SEGA (3a) prevents indomethacin (NSAID)-induced mitochondrial oxidative stress (MOS) and dysfunctions in gastric mucosal cells, which play a pathogenic role in inducing gastropathy. SEGA (3a) offers this mitoprotective effect by scavenging of mitochondrial superoxide anion (O2.-) and intramitochondrial free iron released as a result of MOS. SEGA (3a) in vivo blocks indomethacin-mediated MOS, as is evident from the inhibition of indomethacin- induced mitochondrial protein carbonyl formation, lipid peroxidation, and thiol depletion. SEGA (3a) corrects indomethacin-mediated mitochondrial dysfunction in vivo by restoring defective electron transport chain function, collapse of transmembrane potential, and loss of dehydrogenase activity. SEGA (3a) not only corrects mitochondrial dysfunction but also inhibits the activation of the mitochondrial pathway of apoptosis by indomethacin. SEGA (3a) inhibits indomethacin-induced down-regulation of bcl-2 and up-regulation of bax genes in gastric mucosa. SEGA (3a) also inhibits indometacin-induced activation of caspase-9 and caspase-3 in gastric mucosa. Besides the gastroprotective effect against NSAID, SEGA (3a) also expedites the healing of already damaged gastric mucosa. Radiolabeled (99mTc- labeled SEGA (3a)) tracer studies confirm that SEGA (3a) enters into mitochondria of gastric mucosal cell in vivo, and it is quite stable in serum. Thus, SEGA (3a) bears an immense potential to be a novel gastroprotective agent against NSAID-induced gastropathy.
REACTIONS WITH INDOLE DERIVATIVES, XLVIII. A Simple Synthesis of Staurosporine Aglycon
Sarstedt, Burkhard,Winterfeldt, Ekkehard
, p. 469 - 476 (2007/10/02)
The staurosporine aglycon is prepared from tryptamine and β-indole acetic acid in two consecutive cyclization reactions.
