Brassica juncea L. (Mustard) Extract Silver NanoParticles and Knocking off Oxidative Stress, ProInflammatory Cytokine and Reverse DNA Genotoxicity

Biomolecules. 2020 Dec 9;10(12):1650. doi: 10.3390/biom10121650.

Abstract

Detoxification is one of the main vital tasks performed by the liver. The purpose of this study was to investigate whether mustard in its normal or nanoparticles could confer a protective/therapeutic effect against TAA-induced acute liver failure in experimental animal models. Mustard ethanolic extract was analyzed by HPLC/MS. To induce liver failure, male rats were injected with 350 mg/kg bw TAA IP, then treated orally with a dose of 100 mg/kg for 15 d of mustard extract and its nanoform before and following induction. The levels of serum liver functions, total cholesterol (TCHo), total glyceride (TG), total bilirubin (TBIL), hepatic malonaldhyde (MDA) and nitric oxide (NO),glutathione (GSH), sodium oxide dismutase (SOD), as well as tumor necrosis factor (TNF-α,) and interleukin 6 (IL-6), were estimated. DNA genotoxicity and hepatic pathology, and immunohistologic (IHC) changes were assayed. The antioxidant content of Phenolic acids, flavonoids in mustard ethanolic extract substantially decreased the levels of ALT, AST, ALP and rehabilitated the histopathological alterations. In addition, nanoforms of mustard ethanol extract have notably increased the levels of GSH, SOD and significantly reduced the levels of MDA. The expression levels of TNF-α and IL-6 in serum and tissue were markedly downregulated. DNA genotoxicity was significantly reversed. Mustard introduced a protective and medicinal effect against TAA in both its forms.

Keywords: Brassica juncea L. seeds extract; DNA genotoxicity; LC/MS; Thioacetamide (TAA); acute liver toxicity; phenolic compounds; pro-inflammatory cytokine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Animals
  • Antioxidants / chemistry
  • Antioxidants / pharmacology*
  • Bilirubin / blood
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / pathology
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Cholesterol / blood
  • DNA Damage
  • Drug Administration Schedule
  • Glutathione / agonists
  • Glutathione / metabolism
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Malondialdehyde / antagonists & inhibitors
  • Malondialdehyde / metabolism
  • Metal Nanoparticles / administration & dosage*
  • Metal Nanoparticles / chemistry
  • Mustard Plant / chemistry*
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / metabolism
  • Oxidative Stress / drug effects
  • Plant Extracts / chemistry
  • Rats
  • Rats, Wistar
  • Silver / chemistry
  • Silver / pharmacology*
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Thioacetamide / administration & dosage
  • Thioacetamide / antagonists & inhibitors
  • Triglycerides / blood
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antioxidants
  • Il6 protein, rat
  • Interleukin-6
  • Plant Extracts
  • Triglycerides
  • Tumor Necrosis Factor-alpha
  • Thioacetamide
  • Nitric Oxide
  • Silver
  • Malondialdehyde
  • Cholesterol
  • Superoxide Dismutase
  • Glutathione
  • Bilirubin