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Cytoprotective propensity of green tea polyphenols against citrinin-induced skeletal-myotube damage in C2C12 cells.

Authors
  • Sharath Babu, G R1
  • Ilaiyaraja, N1
  • Khanum, Farhath1
  • Anand, T2
  • 1 Biochemistry and Nano Sciences Division, Defence Food Research Laboratory, Mysuru, Karnataka, 570011, India. , (India)
  • 2 Biochemistry and Nano Sciences Division, Defence Food Research Laboratory, Mysuru, Karnataka, 570011, India. [email protected] , (India)
Type
Published Article
Journal
Cytotechnology
Publication Date
Aug 01, 2017
Volume
69
Issue
4
Pages
681–697
Identifiers
DOI: 10.1007/s10616-017-0077-4
PMID: 28536872
Source
Medline
Keywords
License
Unknown

Abstract

The mycotoxin citrinin, is produced by several species of Penicillium, Aspergillus and Monascus, and is capable of inducing cytotoxicity, oxidative stress and apoptosis. The aim of the present study was to investigate the effect of citrinin in mouse skeletal muscle cells (C2C12) and to overcome the cellular adverse effects by supplementing green tea extract (GTE) rich in polyphenols. C2C12 myoblasts were differentiated to myotubes and were exposed to citrinin in a dose dependent manner (0-100 µM) for 24 h and IC50 value was found to be 100 µM that resulted in decreased cell viability, increased LDH leakage and compromised membrane integrity. Mitochondrial membrane potential loss, increased accumulation of intracellular ROS and sub G1 phase of cell cycle was observed. To ameliorate the cytotoxic effects of CTN, C2C12 cells were pretreated with GTE (20, 40, 80 µg/ml) for 2 h followed by citrinin (100 µM) treatment for 24 h. GTE pretreatment combated citrinin-induced cytotoxicity and oxidative stress. GTE at 40 and 80 µg/ml significantly promoted cell survival and upregulated antioxidant enzyme activities (CAT, SOD, GPx) and endogenous antioxidant GSH, while the gene and protein expression levels were significantly restored through its effective antioxidant mechanism. Present study results suggested the antioxidant properties of GTE as a herbal source in ameliorating the citrinin-induced oxidative stress.

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