Estrogen supplementation failed to attenuate biochemical indices of neutrophil infiltration or damage in rat skeletal muscles following ischemia

Tiidus, Peter M.; Deller, Mirada; Bombardier, Éric; Gül, Mustafa; Liu, X. Linda

doi:10.4067/s0716-97602005000200011

Cited by 11 publications

(13 citation statements)

References 32 publications

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“…21,35 To date, only female animals have been used in animal-model investigations of the potential beneficial effects of E2 for peripheral arterial disease, so we sought to extend these studies to male animals by administering E2 to male mice with HLI. Surgical induction of HLI is a common and reliable method for modeling peripheral arterial disease, [36][37][38][39][40] and because ischemia occurs in the limb, rather than in the heart, functional recovery can be easily monitored by using LDPI to measure blood flow. Functional data is much more difficult to obtain in models of cardiovascular diseases such as myocardial ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia

et al. 2009

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We investigated whether administration of estradiol to male mice augments mobilization of bone marrow-derived endothelial progenitor cells (EPC) and incorporation into foci of neovascularization after hind-limb ischemia, thereby contributing to blood flow restoration. Mice were randomized and implanted with placebo pellets or pellets containing low-dose estradiol (0.39 mg) or high-dose estradiol (1.7 mg). Hind-limb ischemia was induced by unilateral resection of the left femoral artery 1 week after pellet implantation, then EPC mobilization and functional recovery was evaluated. EPC recruitment was assessed in mice transplanted with bone marrow from transgenic donors expressing β-galactosidase driven by the Tie-2 promoter. EPC culture assay performed 2 weeks after pellet implantation revealed a significantly greater (p < 0.05) number of circulating EPCs in the high-dose estradiol group than in the low-dose estradiol and placebo groups. At 3 and 4 weeks after induction of hindlimb ischemia, perfusion was significantly greater (p < 0.05) in high-dose estradiol mice than in mice implanted with the low-dose estradiol or placebo pellets. At 1 and 4 weeks after hind-limb ischemia surgery, more bone marrow-derived EPCs, identified as β-galactosidase-positive cells, were observed in ischemic regions from highdose estradiol animals than in low-dose (p < 0.05) or placebo groups (p < 0.05). These results indicate that estradiol dose-dependently increases the levels of EPCs in peripheral blood in male animals, improves the recovery of blood flow, and decreases limb necrosis after hind-limb ischemia, and that this enhancement occurs, in part, through augmentation of EPC mobilization and greater incorporation of bone marrow-derived EPCs into foci of neovascularization.

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Section: Discussionmentioning

confidence: 99%

Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia

et al. 2009

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“…; Tiidus et al . ), but injury markers were increased in one study (Tiidus et al . ), and unchanged in two (MacIntyre et al .…”

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confidence: 92%

“…Exercise or a bout of eccentric contractions was used to induce the injury in all but five of the 19 studies; in those five studies, injury was induced via a toxin injection or hindlimb ischaemia–reperfusion (Stupka & Tiidus, ; Tiidus et al . ; McHale et al . ; Velders et al .…”

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confidence: 99%

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A moderate oestradiol level enhances neutrophil number and activity in muscle after traumatic injury but strength recovery is accelerated

Novotny

Mader

et al. 2018

The Journal of Physiology

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Oestrogen has been shown to protect against skeletal muscle injury and a reduced inflammatory response has been suggested as a possible protective mechanism. There are, however, dissenting reports. Our objective was to conduct an unbiased, comprehensive study of the effect of oestradiol on the inflammatory response following muscle injury. Female C57BL6/J mice were ovariectomized and supplemented with and without oestradiol. Tibialis anterior muscles were freeze injured and studied primarily at 1-4 days post-injury. Oestradiol supplementation increased injured muscle gene expression of neutrophil chemoattractants (Cxcl1 and Cxcl5) and to a lesser extent that of monocyte/macrophage chemoattractants (Ccl2 and Spp1). Oestradiol markedly increased gene expression of the neutrophil cell surface marker (Ly6g) but had less consistent effects on the monocyte/macrophage cell surface markers (Cd68, Cd163 and Cd206). These results were confirmed at the protein level by immunoblot with oestradiol increasing LY6G/C content and having no significant effect on CD163 content. These findings were confirmed with fluorescence-activated cell sorting counts of neutrophils and macrophages in injured muscles; oestradiol increased the proportion of CD45 cells that were neutrophils (LY6G ) but not the proportion that were macrophages (CD68 or CD206 ). Physiological impact of the oestradiol-enhanced neutrophil response was assessed by strength measurements. There was no significant difference in strength between oestradiol-supplemented and -unsupplemented mice until 2 weeks post-injury; strength was 13-24% greater in supplemented mice at 2-6 weeks post-injury. In conclusion, a moderate level of oestradiol supplementation enhances neutrophil infiltration in injured muscle and this is associated with a beneficial effect on strength recovery.

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“…Moreover, procedures such as removal of neutrophils by an antiserum (Tepperman et al, 1993) or prevention of neutrophil adherence by anti-Mol monoclonal antibody (Simpson et al, 1988), have been demonstrated to protect against gastric mucosa injury induced by I/R. MPO activity was a marker to assay neutrophil infiltrations (Tiidus et al, 2005). In the present study, we observed a significant increase in MPO activity in the stomach after I/R, which was in agreement with previous research (Gou et al, 2011;Kobata et al, 2007), confirming the infiltration and activation of neutrophils in the gastric mucosa during I/R.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Liu

Gou

et al. 2013

Pharmaceutical Biology

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Context: Rutin, a flavonoid commonly present in onions, apples and tea, has been suggested to have a variety of pharmacological activities, including immunomodulator, anti-inflammatory and antioxidant activities. Objectives: The present study was to examine the protective effects of rutin on gastric mucosal damage induced by gastric ischemia-reperfusion (I/R) in rats. Materials and methods: Rutin (50, 100, 200 mg/kg) was administered intragastrically for five consecutive days before ischemia. Sixty minutes after the last administration of rutin, under anesthesia, the celiac artery was clamped for 30 min, and then the clamp was removed for 60 min reperfusion. After reperfusion, the stomach was removed for biochemical and histological examinations. Results: As compared with the I/R group (116.7 AE 21.5), administration of rutin at doses of 50, 100 and 200 mg/kg significantly prevented the increase of gastric mucosal injury index induced by gastric I/R (73.4 AE 14.8, 65.9 AE 9.6 and 26.9 AE 5.7, respectively). ED 50 value was 138.7 mg/kg. Moreover, rutin at doses of 50, 100 and 200 mg/kg showed an inhibition on the increased myeloperoxidase (24.6, 41.3 and 53.1% reduction) activity and malondialdehyde levels (27.4, 40.3 and 50.7% reduction) in gastric mucosa. Also, the elevation of inducible NO synthase (iNOS) activity as well as the decrease of constitutive NO synthase (cNOS) in the gastric mucosa were significantly prevented by rutin pretreatment. Conclusion: These results suggested that rutin has a protective effect against gastric mucosal injury induced by gastric I/R and that the gastroprotection was related to the NOS/NO pathway and its antioxidant activity.

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Estrogen supplementation failed to attenuate biochemical indices of neutrophil infiltration or damage in rat skeletal muscles following ischemia

Cited by 11 publications

References 32 publications

Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia

Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia

A moderate oestradiol level enhances neutrophil number and activity in muscle after traumatic injury but strength recovery is accelerated

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

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