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Molecular docking, pharmacokinetic studies, and in vivo pharmacological study of indole derivative 2-(5-methoxy-2-methyl-1H-indole-3-yl)-N′-(E)-(3-nitrophenyl) methylidene acetohydrazide as a promising chemoprotective agent against cisplatin induced organ damage
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Molecular docking, pharmacokinetic studies, and in vivo pharmacological study of indole derivative 2-(5-methoxy-2-methyl-1H-indole-3-yl)-N′-(E)-(3-nitrophenyl) methylidene acetohydrazide as a promising chemoprotective agent against cisplatin induced organ damage
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Molecular docking, pharmacokinetic studies, and in vivo pharmacological study of indole derivative 2-(5-methoxy-2-methyl-1H-indole-3-yl)-N′-(E)-(3-nitrophenyl) methylidene acetohydrazide as a promising chemoprotective agent against cisplatin induced organ damage
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Journal Article
Molecular docking, pharmacokinetic studies, and in vivo pharmacological study of indole derivative 2-(5-methoxy-2-methyl-1H-indole-3-yl)-N′-(E)-(3-nitrophenyl) methylidene acetohydrazide as a promising chemoprotective agent against cisplatin induced organ damage
2021
Overview
Cisplatin is an efficient anticancer drug against various types of cancers however, its usage involves side effects. We investigated the mechanisms of action of indole derivative, 2-(5-methoxy-2-methyl-1H-indol-3-yl)-N'-[(E)-(3-nitrophenyl) methylidene] acetohydrazide (MMINA) against anticancer drug (cisplatin) induced organ damage using a rodent model. MMINA treatment reversed Cisplatin-induced NO and malondialdehyde (MDA) augmentation while boosted the activity of glutathione peroxidase (GPx), and superoxide dismutase (SOD). The animals were divided into five groups (
n
= 7). Group1: Control (Normal) group, Group 2: DMSO group, Group 3: cisplatin group, Group 4: cisplatin + MMINA group, Group 5: MMINA group. MMINA treatment normalized plasma levels of biochemical enzymes. We observed a significant decrease in CD4
+
COX-2, STAT3, and TNF-α cell population in whole blood after MMINA dosage. MMINA downregulated the expression of various signal transduction pathways regulating the genes involved in inflammation i.e.
NF-κB, STAT-3, IL-1, COX-2, iNOS, and TNF-α
. The protein expression of these regulatory factors was also downregulated in the liver, kidney, heart, and brain. In silico docking and dynamic simulations data were in agreement with the experimental findings. The physiochemical properties of MMINA predicted it as a good drug-like molecule and its mechanism of action is predictably through inhibition of ROS and inflammation.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 631/337
/ 631/67
/ Animals
/ Antineoplastic Agents - administration & dosage
/ Antineoplastic Agents - adverse effects
/ Antioxidants - administration & dosage
/ Antioxidants - pharmacokinetics
/ Cancer
/ Cisplatin - administration & dosage
/ Dosage
/ Glutathione Peroxidase - metabolism
/ Humanities and Social Sciences
/ Indoles
/ Indoles - administration & dosage
/ Inflammation - chemically induced
/ Kidneys
/ Male
/ Malondialdehyde - metabolism
/ Molecular Docking Simulation
/ Oxidative Stress - drug effects
/ Rats
/ Reactive Oxygen Species - metabolism
/ Science
/ Signal Transduction - drug effects
