The effects of lycopene on intestinal injury due to methotrexate in rats
Objective: The aim of this study was to investigate the effects of lycopene (Lyc) on methotrexate (Mtx)-induced intestinal damage in rats. Method: Twenty-eight male Sprague Dawley rats were divided into four equal groups: control, Mtx, Lyc, and Mtx-L. Control group: Rats were given only the vehicle....
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Veröffentlicht in: | Redox report : communications in free radical research 2016-05, Vol.21 (3), p.113-118 |
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Sprache: | eng |
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Zusammenfassung: | Objective: The aim of this study was to investigate the effects of lycopene (Lyc) on methotrexate (Mtx)-induced intestinal damage in rats.
Method: Twenty-eight male Sprague Dawley rats were divided into four equal groups: control, Mtx, Lyc, and Mtx-L.
Control group: Rats were given only the vehicle.
Lyc group: Rats were given Lyc (10 mg/kg) with corn oil by oral gavage for 10 days.
Mtx group: Rats were injected intraperitoneally with a single dose of 20 mg/kg of Mtx and given corn oil by oral gavage.
Mtx-L group: Rats were treated with Lyc (10 mg/kg) for 10 days after a single dose of Mtx (20 mg/kg). All of the rats were euthanized using terminal anesthesia, and the intestinal tissues were removed for histological examination and for pro-inflammatory cytokine measurement (tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β)), total oxidative status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI).
Results: Mtx administration increased histopathological damage and increased TNF-α, IL-1β, TOS, TAC, and OSI levels in the small intestine tissues. Lyc therapy applied to the Mtx-L group provided significant improvement in all parameters of histopathological damage to the small intestine and significantly reduced the levels of IL-1β, TOS, and OSI in the intestinal tissues.
Conclusions: The results of this study indicate that Lyc might be useful for protecting intestinal damage induced by Mtx in rats by reducing the increased oxidative stress and pro-inflammatory cytokine (IL-1β) levels. |
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ISSN: | 1351-0002 1743-2928 |
DOI: | 10.1179/1351000215Y.0000000041 |