title: Ischemic preconditioning and tacrolimus pretreatment as strategies to attenuate intestinal ischemia-reperfusion injury in mice.
abstract: The intestine is highly sensitive to ischemia-reperfusion injury (IRI), a phenomenon occurring in different intestinal diseases. Several strategies to mitigate IRI are in experimental stages; unfortunately, no consensus has been reached about the most appropriate one. We report a protocol to study ischemic preconditioning (IPC) evaluation in mice and to combine IPC and tacrolimus (TAC) pretreatment in a warm ischemia model. Mice were divided into treated (IPC, TAC, and IPC + TAC) and untreated groups before intestinal ischemia. IPC, TAC, and IPC + TAC groups were able to decrease postreperfusion nitrites levels (P < .05). IPC-containing groups had a major beneficial effect by preserving the integrity of the intestinal histology (P < .05) and improving animal survival (P < .002) compared with TAC alone or the untreated group. The IPC + TAC group was the only one that showed significant improvement in lung histological analysis (P < .05). The TAC and IPC + TAC groups down-regulated intestinal expression of interleukin (II)-6 and IL1b more than 10-fold compared with the control group. Although IPC and TAC alone reduced intestinal IRI, the used of a combined therapy produced the most significant results in all the local and distant evaluated parameters.
authors: Laboratorio de Microcirugía Experimental, Instituto de Trasplante Multiorgánico, Hospital Universitario Fundación Favaloro, Buenos Aires, Argentina. pablo_stringa@hotmail.com
authors: P
authors: P
authors: Stringa
authors: D
authors: D
authors: Romanin
authors: N
authors: N
authors: Lausada
authors: M
authors: M
authors: Machuca
authors: J C
authors: JC
authors: Raimondi
authors: A
authors: A
authors: Cabanne
authors: M
authors: M
authors: Rumbo
authors: G
authors: G
authors: Gondolesi
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003131:Combined Modality Therapy; D004195:Disease Models, Animal; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007410:Intestinal Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology; D019194:Ischemic Preconditioning; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009573:Nitrites / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D016559:Tacrolimus / Q000494:pharmacology*; D013997:Time Factors; D052096:Warm Ischemia / Q000009:adverse effects
chemical_list: D015415:Biomarkers; C587672:IL1B protein, mouse; D007166:Immunosuppressive Agents; D053583:Interleukin-1beta; D015850:Interleukin-6; D009573:Nitrites; C577686:interleukin-6, mouse; D016559:Tacrolimus