ArticleAnnals of translational medicine2020
Lipoxin A4 protects rat skin flaps against ischemia-reperfusion injury through inhibiting cell apoptosis and inflammatory response induced by endoplasmic reticulum stress.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The effect of KUS121, a novel VCP modulator, against ischemic injury in random pattern flaps.PloS one · 2024Article
- Microvascular Fragments Protect Ischemic Musculocutaneous Flap Tissue from Necrosis by Improving Nutritive Tissue Perfusion and Suppressing Apoptosis.Biomedicines · 2023Article
- Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Exploration of the Protective Mechanism of Bax Removal against Ischemia Reperfusion Injury of Skin Flap through the p38 Mitogen-Activated Protein Kinase Pathway.Oxidative medicine and cellular longevity · 2022Article
- Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps.Frontiers in pharmacology · 2022Article
- Improving the ischemia-reperfusion injury in vascularized composite allotransplantation: Clinical experience and experimental implications.Frontiers in immunology · 2022Review
- Targeting GRP78 enhances the sensitivity of HOS osteosarcoma cells to pyropheophorbide-α methyl ester-mediated photodynamic therapy via the Wnt/β-catenin signaling pathway.Acta biochimica et biophysica Sinica · 2021Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ischemia-reperfusion (I/R) injury of skin flap is a complex pathophysiological process involving many cells and factors. Although endoplasmic reticulum (ER) stress-induced cell apoptosis and inflammatory response are of immense importance in the skin flap ischemia, the treatment for I/R injury induced by ER stress is barely reported.
methodsHealthy male Wister rats were randomly divided into three groups: sham-operated group, I/R model group and I/R + LXA4 group. I/R-induced injury in skin flaps with or without pre-treatment of Lipoxin A4 (LXA4, 100 µg/kg) was tested by using HE and TUNEL staining. Related factors associated with oxidative stress, apoptosis, inflammatory response, and ER stress were tested by ELISA, biochemical assay, and western blotting, respectively.
resultsOur results showed that LXA4 treatment significantly promotes skin flap survival and attenuates I/R injury by inhibiting oxidative stress, apoptosis, and inflammatory factor release, evidenced by the decreased expression of malondialdehyde (MDA), lactate dehydrogenase (LDH), NF-κBp65, tumor necrosis factor α (TNF-α), ET, active Caspase-3 and Bax and up-regulated superoxide dismutase (SOD), glutathione (GSH) level and Bcl-2 expression. Moreover, LXA4 treatment also reverses the increased expression of GRP78, p-PERK, p-eIF2α, ATF4, and CHOP induced by I/R injury.
conclusionsIn conclusion, we showed that ER stress causes cell apoptosis and inflammatory response, resulting in the skin flaps injury. LXA4 exhibits a protective effect on skin flaps against I/R injury through the inhibition of ER stress.
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