Mitochondrial proteomic analysis of isopsoralen protection against oxidative damage in human lens epithelial cells.
- Author:
Chun-Yan FENG
1
;
Xiu-Rong HUANG
;
Ming-Xin QI
;
Song-Wen TANG
;
Yan-Hong HU
;
Sheng CHEN
;
Fa-Jie KE
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Epithelial Cells; drug effects; metabolism; pathology; Estradiol; pharmacology; Furocoumarins; pharmacology; Humans; Hydrogen Peroxide; toxicity; Lens, Crystalline; pathology; Mitochondria; metabolism; Oxidation-Reduction; drug effects; Oxidative Stress; drug effects; Protective Agents; pharmacology; Proteome; metabolism; Proteomics; methods
- From: Chinese journal of integrative medicine 2012;18(7):529-533
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the protective effects of the natural medicinal monomer isopsoralen (ISR) with estrogenic activity against oxidative damage in human lens epithelial cells B3 (HLE-B3) caused by hydrogen peroxide (H(2)O(2)) and to pursue the possible mitochondrial proteomic regularity of the protective effects.
METHODSHLE-B3 cells were treated with H(2)O(2) (300 μ mol/L), β-estradiol (E(2): 10(-8) mol/L) and H(2)O(2), ISR (10(-5) mol/L) and H(2)O(2), or left untreated. Altered expressions of all mitochondrial proteins were analyzed by protein array and surfaceenhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS). The mass/charge (m/z) ratios of each peak were tested by the Kruskal-Wallis rank sum test, and the protein peak value of the m/z ratio for each treatment by pair comparison was analyzed with the Nemenyi test.
RESULTSH(2)O(2) up-regulated the expressions of two protein spots (with m/z of 6532 and 6809). E(2) mitigated the oxidative damage, and the expression of one protein spot (m/z 6532) was down-regulated. In contrast, ISR down-regulated both of protein spots (m/z 6532 and 6809).
CONCLUSIONSISR could effectively inhibit H(2)O(2)-induced oxidative damage in HLE-B3 cells. The protein spot at m/z of 6532 might be the target spot of ISR against oxidative damage induced by H(2)O(2).