[The protective effect of lycopene on lung oxidative damage induced by atmospheric fine particulate matter exposure in rats].

Abstract

Objective: To investigate the protective effect of lycopene on lung oxidative damage induced by atmospheric fine particulate matter(PM_(2.5)) in rats.

Methods: Sixty 7-week-old male Sprague-Dawley rats were randomly divided into six groups: normal control group, PM_(2.5) model group, reference control group(vitamin E dose group, 7.5 mg/kg), and three lycopene groups with low-dose(5 mg/kg), medium dose(15 mg/kg) and high dose(30 mg/kg), with 10 rats in each group. Except for the control group, all groups were exposed to PM_(2.5) suspension intratracheally(equivalent to 7.5 mg/kg), poisoning 3 times a week, with an interval of 24 hours between each test. The vitamin E intervention group dissolved the salad oil with vitamin E by daily gavage, while the control group received an equal amounts of physiological saline. From the first day of exposure, lycopene was given daily via gavage for 4 weeks. Lycopene groups received lycopene dissolved in salad oil, while control and model groups received salad oil of the same volume. After 4 weeks, all rats were killed. Lung pathology sections were made and serum and lung tissue were collected and homogenized, centrifuge and collect the supernatant. Using UV visible spectrophotometry to measure levels of glutathione peroxidase(GSH-Px), glutataione(GSH), superoxide dismutase(SOD), total antioxidant capacity(T-AOC), malondialdehyde(MDA), glutathione S-transferase(GST), catalase(CAT), hydroxyl radical(OH), nitric oxide(NO). Using enzyme-linked immunosorbent Assays(ELISA) to measure levels of tumor necrosis facto-α(TNF-α), interleukin-6(IL-6), and 8-hydroxy-2-deoxyguanosine(8-OHdG). Lung histopathology was also observed.

Results: Compared to the normal control group, there were significant differences in the content of GSH((9.47±1.37)mg/g vs. (11.10±3.82)mg/g), SOD((9.43±2.41)U/mg vs. (13.82±4.64)U/mg), CAT((5.35±1.88)U/mg vs. (9.54±3.06)U/mg), 8-OHdG((5.52±1.66)μg/g vs. (4.76±1.01)μg/g) in the serum, and GSH((2.19±0.29)mg/g vs. (3.18±0.49)mg/g), SOD((23.98±4.20)U/mg vs. (31.95±5.08)U/mg), CAT((5.85±1.95)U/mg vs. (3.57±1.96)U/mg), GSH-Px((49.15±7.01)mg/g vs. (68.46±11.15)mg/g), OH·((74.02±12.84)U/mg vs. (51.03±14.85)U/mg), TNF-α((5.57±0.72)ng/g vs. (7.83±1.60)ng/g), IL-6((2.68±0.39)μg/g vs. (3.82±1.35)μg/g) in lung tissue homogenates of PM_(2.5) group(P<0.05). These indicated that there were oxidative damage to the body. Compared to the PM_(2.5) group, there were significant differences in the content of GSH((10.57±2.88)mg/g vs. (9.47±1.37)mg/g), SOD((13.51±2.95)U/mg vs. (9.43±2.41)U/mg), 8-OHdG((4.38±0.26)μg/g vs. (5.52±1.66)μg/g) in the serum and GSH((2.72±0.49)mg/g vs. (2.19±0.29)mg/g), GSH-Px((63.46±17.03)mg/g vs. (49.15±7.01)), CAT((3.72±1.28)U/mg vs. (5.85±1.95)U/mg), OH·((65.73±14.88)U/mg vs. (74.02±12.84)U/mg), NO((3.83±1.60)μmol/mg vs. (2.48±1.49)μmol/mg), TNF-α((7.49±1.28)ng/g vs. (5.57±0.72)ng/g), IL-6((3.77±1.35)μg/g vs. (2.68±0.39)μg/g) in lung tissue homogenates of the high-dose lycopene group(P<0.05); the content of GSH((10.57±2.88)mg/g vs. (9.43±2.41)mg/g), CAT((10.61±4.41)U/mg vs. (5.35±1.88)mg/g) in the serum, and GSH((2.77±0.75)mg/g vs. (2.19±0.29)mg/g), SOD((30.88±9.65)U/mg vs. (23.98±4.20)U/mg), CAT((4.52±1.30)U/mg vs. (5.85±1.95)U/mg), TNF-α((7.37±2.50)ng/g vs. (5.57±0.72)ng/g), IL-6((3.80±1.36)μg/g vs. (2.68±0.39)μg/g) in lung tissue homogenates of the medium-dose group(P<0.01). the content of GSH((10.64±2.71)mg/g vs. (9.47±1.37)mg/g), SOD((13.51±2.95)U/mg vs. (9.43±2.41)U/mg) in the serum, and OH·((67.29±16.11)U/mg vs. (74.02±12.84)U/mg) in lung tissue homogenates of the vitamin E group(P<0.05). The PM_(2.5) group had alveolar structure destruction, alveolar septal thickening, pulmonary interstitial oedema, inflammatory infiltration. In the lycopene high-dose intervention group had intact alveolar structure, with a few neutrophil infiltration inside and outside the bronchiolar lumen, the aggregation degree of inflammatory cells was lower than that of the PM_(2.5) group, blood vessels were slightly dilated and congested, and the pulmonary interstitium was slightly widened, medium dose and low dose of lycopene are more obvious. In the vitamin E group performed similar to the lycopene medium-dose intervention group. suggesting a protective effect of lycopene on lung tissue integrity.

Conclusion: Lycopene exhibits protective effects against PM_(2.5)-induced oxidative lung damage, likely through its enhancement of antioxidant enzyme activities, reduction of free radical-induced oxidative damage, and stabilization of biological membranes.