The effects of zinc chloride (ZnCl2), disodium zinc ethylenediamine tetraacetate (Zn-EDTA), and zinc gluconate (Zn-GLU) on the antioxidant enzyme activities and levels of interleukins (ILs) in psoriasis-induced mice were studied. One hundred twenty female mice were randomly divided into six groups with 20 mice in each group: the control, positive control (PC), methotrexate (MTX), ZnCl2, Zn-EDTA, and Zn-GLU groups. All animals except the control group were given diethylstilbestrol for three consecutive days. After successfully inducing psoriasis, the control and PC groups were given normal saline (i.g.) daily while the remaining groups were given MTX, ZnCl2, Zn-EDTA, and Zn-GLU, respectively. The results revealed that the zinc supplementation could significantly (p < 0.05) inhibit mitosis in the mouse vaginal epithelium as methotrexate did and the inhibiting efficacy had nothing to do with the zinc forms. After ZnCl2, Zn-EDTA, and Zn-GLU supplementation, the levels of liver superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities increased and the concentration of malondialdehyde (MDA) decreased significantly (p < 0.05) compared to the PC group. The levels of SOD, CAT activity, and MDA level between each zinc supplementation group and MTX group were insignificant (p > 0.05). The zinc treatments also caused a significant (p < 0.05) decrease in the raised IL-2 level of animal serum. The results obtained in the present work indicate the potential for zinc as a complementary pharmaceutical intervention for the treatment of topical psoriasis.
Background: Hemorrhagic shock-induced ischemia and hypoxia elicit endoplasmic reticulum stress (ERS) that leads to cell apoptosis, tissue structural damage and organ dysfunction and failure. Stellate ganglion blockade (SGB) has been demonstrated to improve intestinal barrier dysfunction induced by hemorrhagic shock. The present study sought to investigate whether the beneficial effect of SGB on the intestinal mucosal barrier function is via suppression of ERS. Materials and methods: A conscious rat model of hemorrhagic shock (40 ±2 mmHg for 1 hour, followed by resuscitation) was established. The parameters reflecting intestinal morphology and intestinal mucosal barrier function including wet-dry ratio (W/D), intestinal permeability, D-lactic acid (D-LA) and intestinal fatty acid binding protein (I-FABP) in plasma, and expressions of ATF6α, PERK, and IRE1α in intestinal tissues were then observed. Furthermore, the effects of either SGB or ERS inhibitor, 4-phenylbutyric acid (4-PBA), on these parameters in rats with hemorrhagic shock were assessed. The effect of ERS agonist tunicamycin (TM) on the rats subjected with both SGB and hemorrhagic shock was also determined. Results: Either SGB or administration of ERS inhibitor, 4-PBA, alleviated hemorrhagic shock-induced adverse effects such as intestinal mucosal barrier dysfunction and excessive autophagy, which were characterized by damaged intestinal tissue, enhanced intestinal permeability and D-LA and I-FABP levels in plasma, and increased expressions of ATF6α, PERK, IRE1α in intestinal tissue. In contrast, administration of ERS agonist, TM, suppressed the beneficial effects of SGB on intestinal tissue and function during hemorrhagic shock. Conclusion: The SGB repairs intestinal mucosal barrier through suppression of ERS following hemorrhagic shock.
The aim is to investigate that 17β-estradiol (E2)/estrogen receptors (ERs) activation normalizes splenic CD4 + T lymphocytes proliferation and cytokine production through inhibition of endoplasmic reticulum stress (ERS) following hemorrhage. The results showed that hemorrhagic shock (hemorrhage through femoral artery, 38–42 mmHg for 90 min followed by resuscitation of 30 min and subsequent observation period of 180 min) decreased the CD4+ T lymphocytes proliferation and cytokine production after isolation and incubation with Concanavalin A (5 μg/mL) for 48 h, induced the splenic injury with evidences of missed contours of the white pulp, irregular cellular structure, and typical inflammatory cell infiltration, upregulated the expressions of ERS biomarkers 78 kDa glucose-regulated protein (GRP78) and activating transcription factor 6 (ATF6). Either E2, ER-α agonist propyl pyrazole triol (PPT) or ERS inhibitor 4-Phenylbutyric acid administration normalized these parameters, while ER-β agonist diarylpropionitrile administration had no effect. In contrast, administrations of either ERs antagonist ICI 182,780 or G15 abolished the salutary effects of E2. Likewise, ERS inducer tunicamycin induced an adverse effect similarly to that of hemorrhagic shock in sham rats, and aggravated shock-induced effects, also abolished the beneficial effects of E2 and PPT, respectively. Together, the data suggest that E2 produces salutary effects on CD4+ T lymphocytes function, and these effects are mediated by ER-α and GPR30, but not ER-β, and associated with the attenuation of hemorrhagic shock-induced ERS.
Numerous studies have examined the association between interleukin-6 and the pathogenesis of lichen planus (LP)/oral LP (OLP) in various populations; however, there is a lack of systematic analysis. The aim of the present study was to assess this association more precisely, thus a meta-analysis was performed. Case-control studies, which were published up to December 2015, were obtained from PubMed, Embase and the China National Knowledge Infrastructure databases. Data were extracted and pooled mean differences (MDs) with 95% confidence intervals (CIs) were calculated. Ultimately, eight studies were included, comprising 299 LP/OLP cases and 231 control subjects. Overall, the pooled MD for IL-6 was 16.24 (95% CI, 9.84-22.64; =99% for heterogeneity). In the subgroup analysis by ethnicity, a significant increase of the IL-6 expression level was identified among Asian individuals, but not in Caucasian individuals. Thus, IL-6 may be significant in the pathogenesis of LP. However, further studies are required to validate these associations.
Background and objectiveSevere hemorrhagic shock leads to excessive in ammation and immune dysfunction, which resulted in high mortality related to mesenteric lymph return. Recent study showed that stellate ganglion block (SGB) increased survival rate in rats suffered hemorrhagic shock. However, whether SGB ameliorates immune dysfunction induced by hemorrhagic shock, it remains unknown. The aim of present study is therefore to verify the favorable effect of SGB on the proliferation and function of splenic CD4 + T cells isolated from rats underwent hemorrhagic shock, and investigate its mechanism focusing autophagy and PHSML. Materials and methodsMale rats underwent SGB or sham SGB pretreatment and conscious acute hemorrhage followed by resuscitation and multiple treatments. After three hours of resuscitation, splenic CD4 + T cells were isolated for the measurements of proliferation and cytokine production following stimulation with ConA in vitro. Furthermore, the CD4 + T cells isolated from normal rats were treated with post-hemorrhagic shock mesenteric lymph (PHSML) drained from rats treated with SGB or not. And the proliferation, cytokine production and autophagy biomarkers were detected. ResultsHemorrhagic shock reduced CD4 + T cells proliferation and function to produce interleukin (IL)-2, IL-4 and tumor necrosis factor-α-induced protein 8 like 2 (TIPE2). SGB pretreatment or administration of autophagy inhibitor 3-methyladenine (3-MA) signi cantly normalized these indicators. In contrast, administration of autophagy agonist rapamycin (RAPA) or intravenous injection of PHSML inhibited the bene cial effect of SGB on CD4 + T cells obtained from hemorrhagic shocked rats. Furthermore, PHSML incubation decreased the proliferation and cytokine production, increased LC3 II/I and Beclin-1 expressions, and reduced p-PI3K and p-Akt expressions of normal CD4 + T cells. More critically, these adverse effects of PHSML were abolished by 3-MA administration, as well as incubation with PHSML obtained from SGB treated rats. ConclusionsSGB improves splenic CD4 + T cells function following hemorrhagic shock, which is related to the inhibition of PHSML-mediated autophagy.
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