scholarly journals Effects of silk fibroin in murine dry eye

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chae Eun Kim ◽  
Ji Hyun Lee ◽  
Yeung Kyu Yeon ◽  
Chan Hum Park ◽  
JaeWook Yang
Keyword(s):  
Mouse Model ◽  
Silk Fibroin ◽  
Dry Eye ◽  
Lacrimal Gland ◽  
Periodic Acid ◽  
Experimental Models ◽  
Inflammatory Factors ◽  
Periodic Acid Schiff ◽  
Scopolamine Hydrobromide ◽  
Tear Production

AbstractThe study aimed to investigate the effects of silk fibroin in a mouse model of dry eye. The experimental dry eye mouse model was developed using more than twelve-weeks-old NOD.B10.H2bmice exposing them to 30–40% ambient humidity and injecting them with scopolamine hydrobromide for 10 days. Tear production and corneal irregularity score were measured by the instillation of phosphate buffered saline or silk fibroin. Corneal detachment and conjunctival goblet cell density were observed by hematoxylin and eosin or periodic acid Schiff staining in the cornea or conjunctiva. The expression of inflammatory markers was detected by immunohistochemistry in the lacrimal gland. The silk group tear production was increased, and corneal smoothness was improved. The corneal epithelial cells and conjunctival goblet cells were recovered in the silk groups. The expression of inflammatory factors was inhibited in the lacrimal gland of the silk group. These results show that silk fibroin improved the cornea, conjunctiva, and lacrimal gland in the mouse model of dry eye. These findings suggest that silk fibroin has anti-inflammatory effects in the experimental models of dry eye.

scholarly journals Lacrimal Gland Myoepithelial Cells Are Altered in a Mouse Model of Dry Eye Disease

2020 ◽  
Vol 190 (10) ◽  
pp. 2067-2079 ◽  
Author(s):  
Laura García-Posadas ◽  
Robin R. Hodges ◽  
Tor P. Utheim ◽  
Ole Kristoffer Olstad ◽  
Vanessa Delcroix ◽  
...  
Keyword(s):  
Mouse Model ◽  
Dry Eye ◽  
Lacrimal Gland ◽  
Myoepithelial Cells ◽  
Dry Eye Disease ◽  
Eye Disease

scholarly journals Immunomodulative Effects of Chamaecyparis obtusa Essential Oil in Mouse Model of Allergic Rhinitis

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4517
Author(s):  
Seung-Heon Shin ◽  
Mi-Kyung Ye ◽  
Dong-Won Lee ◽  
Mi-Hyun Che
Keyword(s):  
Allergic Rhinitis ◽  
Essential Oil ◽  
Mouse Model ◽  
Periodic Acid ◽  
Chamaecyparis Obtusa ◽  
Staining Procedure ◽  
Periodic Acid Schiff ◽  
Nasal Symptoms ◽  
Tnf Α ◽  
Sinonasal Mucosa

The present study aims to investigate the immunomodulatory effects of essential oil from Chamaecyparis obtusa (EOCO) in an ovalbumin (OVA)-induced allergic rhinitis (AR) mouse model. BALB/c mice were intraperitoneally sensitized and stimulated with OVA. From day 22 to 35, 0.01% and 0.1% ECOC was intranasally administered 1 h before OVA stimulation. Nasal symptoms, as well as serum total and OVA-specific immunoglobulin (Ig) E levels, were measured. Interleukin (IL)-4, IL-10, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels in nasal lavage fluid (NLF) and their production by activated splenocytes were measured. Histological changes in the sinonasal mucosa were evaluated through hematoxylin and eosin and periodic acid-Schiff staining procedure. Th cytokines and their transcription factor mRNA expressions were determined using reverse-transcription polymerase chain reaction. Intranasal EOCO administration significantly suppressed allergic symptoms, OVA-specific IgE level, sinonasal mucosal inflammatory cell infiltration, and mucus-producing periodic acid-Schiff (PAS) positive cell count. EOCO also significantly inhibited IL-4, IL-10, and TNF-α levels in NLF and activated splenocytes. Th2 and Treg related cytokines and their transcription factors in sinonasal mucosa were significantly suppressed through intransal EOCO instillation. In conclusion, repetitive EOCO intranasal instillation showed anti-inflammatory and anti-allergic effects by suppressing nasal symptoms and inhibiting the production and expression of inflammatory mediators in the OVA-induced AR mouse model.

scholarly journals Psoriasis-Like Inflammation Induced Renal Dysfunction through the TLR/NF-κB Signal Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Fang Ren ◽  
Min Zhang ◽  
Caiyun Zhang ◽  
Hong Sang
Keyword(s):  
Renal Injury ◽  
Periodic Acid ◽  
Severity Index ◽  
Skin Lesions ◽  
Signal Pathway ◽  
Inflammatory Factors ◽  
Urine Protein ◽  
Periodic Acid Schiff ◽  
Associated Proteins ◽  
Pas Staining

Pathological studies have shown an association between psoriasis and renal injury (RI), but the mechanism between RI and psoriasis was still unclear. This paper was designed to investigate the relationship and mechanism between psoriasis-like inflammation and renal injury in BALB/C mice. Mice were topically smeared imiquimod followed by various analyses in skin lesions, urine protein, kidney/serum inflammatory cytokines, kidney function, podocyte membrane proteins, and toll-like receptors/nuclear factor kappa-b (TLR/NF-κB) pathway-associated proteins. Meanwhile, lipopolysaccharide (LPS) and dexamethasone (DEX) were intraperitoneally injected to promote and inhibit inflammation accompanied by imiquimod to elaborate the relevance between inflammatory levels and RI. In the model group, the Psoriasis Area and Severity Index (PASI) scores of scaly and erythema obviously increased (p<0.01), creatinine and blood urea nitrogen significantly increased (p<0.01), the positive area of hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining in kidney increased (p<0.01), malondialdehyde significantly increased with superoxide dismutase (SOD) decreased (p<0.01), 24-hour urine protein increased and the expressions of podocin and CD2 associate protein (CD2AP) decreased (p<0.01), and kidney/serum inflammatory factors (IL-17, IL-1β, IL-6, TNF-α, and IL-22) and TLR/NF-κB-related expression (TLR2, TLR4, MyD88, and NF-κBp65) all increased (p<0.01). The RI was aggravated with the TLR/NF-κB related expression being upregulated by LPS (p<0.05). On the contrary, the RI was alleviated by DEX (p<0.05). Our data showed that psoriasis-like inflammation damaged the renal function via the TLR/NF-κB signal pathway. Inhibiting TLR/NF-κB-related protein expression may be effective for the treatment of RI caused by psoriasis.

scholarly journals Electroacupuncture Alleviates Inflammation of Dry Eye Diseases by Regulating the α7nAChR/NF-κB Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Ning Ding ◽  
Qingbo Wei ◽  
Weimin Deng ◽  
Xinyi Sun ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Dry Eye ◽  
Inhibitory Effect ◽  
Cell Ultrastructure ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Scopolamine Hydrobromide ◽  
Beneficial Effects ◽  
Chip Technology

Purpose. We tried to investigate whether electroacupuncture (EA) can reduce inflammation of dry eye disease (DED) by regulating α7nAChR and inhibiting the NF-κB signaling pathway. Methods. Healthy New Zealand white rabbits were treated with scopolamine hydrobromide (Scop) for 21 consecutive days to establish the DED animal model. After 21 days, EA, fluorometholone (Flu), and α7nAChR antagonist (α-BGT) treatments were performed, and the Scop injection was continued until day 35. During treatment, the fluorescence staining of the corneal epithelium and the level of tear flow were observed. The influence of EA on the LG pathology and inflammatory factors ACh, α7nAChR, and NF-κB was detected using the LG histopathology, transmission electron microscopy (TEM), cytokine protein chip technology, enzyme-linked immunosorbent assay (ELISA), and Western blot. Results. The EA stimulation can reduce the corneal epithelial damage and repair epithelial cell ultrastructure, promote the tear secretion, relieve the LG atrophy and decrease lipid droplet accumulation in LG acinar cell, and reduce the levels of inflammatory cytokines (i.e., IL-1, MIP-1b, TNF-α, and IL-8) in the LG. The protective effect of EA on the inflammation and the ocular surface is similar to the corticosteroid Flu. EA and Flu can upregulate the expression of the α7nAChR and downregulate the expression of NF-κB. The α7nAChR antagonist α-BGT can reverse the protective effect of EA on the LG and the inhibitory effect on the NF-κB pathway and the expression of inflammatory factors but cannot affect the expression of Flu on the NF-κB pathway and inflammatory factors. Conclusion. These results prove that EA can alleviate DEDs by stimulating the acupoints around the eyes. These beneficial effects are related to the upregulation of α7nAChR and the downregulation of NF-κB in the LG. The protective effect of LG is mediated through the anti-inflammatory pathway mediated by α7nAChR. EA can reduce the NF-κB P65 nuclear transcription and reduce inflammatory factors by regulating α7nAChR. This expression indicates that the α7nAChR/NF-κB signaling pathway may serve as a potential therapeutic target for EA to treat DEDs.

HPMSCs Inhibit the Expression of PD-1 in CD4+IL-10+ T Cells and Mitigate liver Damage in a GVHD Mouse Model by Regulating the Cross-talk Between Nrf2 and NF-κB Signaling Pathway

2021 ◽  
Author(s):  
Aiping Zhang ◽  
Jiashen Zhang ◽  
Xiaohua Li ◽  
Hengchao Zhang ◽  
Yanlian Xiong ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mouse Model ◽  
Nuclear Translocation ◽  
Periodic Acid ◽  
Cell Generation ◽  
Hepatic Tissue ◽  
Sod Activity ◽  
Periodic Acid Schiff ◽  
Redox Metabolism

Abstract Background: The activation of T cells and imbalanced redox metabolism enhances the development of graft-versus-host disease (GVHD). Human placenta-derived mesenchymal stromal cells (hPMSCs) can improve GVHD through regulating T cell responses. However, whether hPMSCs balance the redox metabolism of CD4+IL-10+ T cells and liver tissue and alleviate GVHD remains unclear. This study aimed to investigate the effect of hPMSC-mediated treatment of GVHD associated with CD4+IL-10+ T cell generation via control of redox metabolism and PD-1 expression and whether the Nrf2 and NF-κB signaling pathways were both involved in the process.Methods: A GVHD mouse model was induced using 6-8-week-old C57BL/6 and Balb/c mice, which were treated with hPMSCs. In order to observe whether hPMSCs affect the generation of CD4+IL-10+ T cells via control of redox metabolism and PD-1 expression, a CD4+IL-10+ T cell culture system was induced using human naive CD4+ T cells. The percentage of CD4+IL-10+ T cells and their PD-1 expression levels were determined in vivo and in vitro using flow cytometry, and Nrf2, HO-1, NQO1, GCLC, GCLM, and NF-κB levels were determined by western blotting, qRT-PCR, and immunofluorescence, respectively. Hematoxylin-eosin, Masson’s trichrome and periodic acid-Schiff staining methods were employed to analyze the changes in hepatic tissue. Results: A decreased activity of superoxide dismutase (SOD) and a proportion of CD4+IL-10+ T cells with increased PD-1 expression were observed in GVHD patients and the mouse model. Treatment with hPMSCs increased SOD activity and GCL and GSH levels in the GVHD mouse model. The percentage of CD4+IL-10+ T cells with decreased PD-1 expression, as well as Nrf2, HO-1, NQO1, GCLC, and GCLM levels, both in the GVHD mouse model and in the process of CD4+IL-10+ T cell generation, were also increased, but NF-κB phosphorylation and nuclear translocation were inhibited after treatment with hPMSCs, which was accompanied by improvement of hepatic histopathological changes.Conclusions: The findings suggested that hPMSC-mediated redox metabolism balance and decreased PD-1 expression in CD4+IL-10+ T cells were achieved by controlling the crosstalk between Nrf2 and NF-κB, which further provided evidence for application of hPMSC-mediated treatment of GVHD.

scholarly journals Resolvin E1 Improves Tear Production and Decreases Inflammation in a Dry Eye Mouse Model

2010 ◽  
Vol 26 (5) ◽  
pp. 431-439 ◽  
Author(s):  
Na Li ◽  
Jiucheng He ◽  
Carl Eric Schwartz ◽  
Per Gjorstrup ◽  
Haydee E.P. Bazan
Keyword(s):  
Mouse Model ◽  
Dry Eye ◽  
Tear Production

scholarly journals The Role of ICOSL Antibody Intervention in Mouse Model of Neutrophil Asthma

2020 ◽  
Author(s):  
Heting DONG ◽  
Yinying Ren ◽  
Yongdong Yan ◽  
Li Huang ◽  
Meijuan Wang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Peripheral Blood ◽  
Periodic Acid ◽  
Immunohistochemical Analysis ◽  
Lavage Fluid ◽  
Periodic Acid Schiff ◽  
Pulmonary Tissue ◽  
Inflammatory Infiltration ◽  
Group I

Abstract Background: To investigate the role of ICOSL (Inducible costimulatory molecular ligands) antibody in the mouse model of neutrophilic asthma, and to explore the role of ICOSL in the pathogenesis of Th1/Th2/Th17 imbalance. Methods: 24 Balb/c mice were randomly divided into four groups: C group, N group, my group and G group. The peripheral blood, BALF and lung tissue were collected within 24 hours after the last challenge. Total count and classification of BALF (bronchoalveolar lavage fluid) cells; Detection cytokines of peripheral blood and BALF. Pulmonary tissue section for pathological observation. Results: During seven stimulations,asthma performance in group N was the earliest and obvious and was improved in group I,there was no asthma behavior in group C.The total number of BALF in N group was the highest, in C group was the lowest,(P<0.05).The concentrations of IL-6, IL-13 and IL-17 in peripheral blood and BALF of N group were the highest,(P<0.05).The IFN-γ concentration of C group was higher than that of N and G groups,(P<0.05).HE(hematoxylin-eosin) and PAS(periodic acid-schiff) staining showed that inflammatory infiltration in I group was relative improved than N and G groups.ICOSL immunohistochemical analysis,ICOSL positive cells of alveolar interstitial and airway of N and G groups were more than I group,(P<0.05). Conclusions: After the intervention of ICOSL antibody,the performance of asthma relieved,and airway inflammatory cell infiltration, mucus secretion were reduced.The levels of IL-6, IL-13 and IL-17 in peripheral blood and BALF were partly decreased, and the level of IFN-γwas increased;These results suggest that blocking the ICOS/ICOSL signaling pathway may partially block the development of neutrophilc asthma and provide a new target for the treatment of asthma.

scholarly journals Alteration in nerves and neurotransmitter stimulation of lacrimal gland secretion in the TSP-1−/− mouse model of aqueous deficiency dry eye

2018 ◽  
Vol 11 (4) ◽  
pp. 1138-1148 ◽  
Author(s):  
Sumit Bhattacharya ◽  
Laura García-Posadas ◽  
Robin R. Hodges ◽  
Helen P. Makarenkova ◽  
Sharmila Masli ◽  
...  
Keyword(s):  
Mouse Model ◽  
Dry Eye ◽  
Lacrimal Gland ◽  
Gland Secretion ◽  
Stimulation Of

scholarly journals A Transplantable Syngeneic Allograft Mouse Model for Nongestational Choriocarcinoma of the Ovary

2019 ◽  
Vol 56 (3) ◽  
pp. 399-403 ◽  
Author(s):  
Ludmila Szabova ◽  
Baktiar Karim ◽  
Melanie Gordon ◽  
Lucy Lu ◽  
Nathan Pate ◽  
...  
Keyword(s):  
Mouse Model ◽  
Periodic Acid ◽  
Treatment Strategies ◽  
Genetically Engineered ◽  
Ovarian Tumors ◽  
Periodic Acid Schiff ◽  
Genetic Mouse Model ◽  
Rare Malignancy ◽  
Schiff Reaction

Nongestational choriocarcinoma is a rare malignancy in humans with poor prognosis. Naturally occurring choriocarcinoma is also rare in laboratory mice, and no genetic mouse model accurately recapitulates the features of this cancer. Here we report development of a genetically engineered mouse (GEM) model with alterations in Brca2, Trp53, and RB that develops ovarian tumors. Most of the ovarian tumors displayed histological characteristics of nongestational choriocarcinoma of the ovary (NGCO) (47%) with abundant syncytiotrophoblasts and cytotrophoblasts, positive immunolabeling for human chorionic gonadotropin, and positive periodic acid–Schiff reaction. The rest of the ovarian tumors were serous epithelial ovarian carcinoma (SEOC) (26%) or mixed tumors consisting of NGCO and SEOC (26%). We further established syngeneic orthotopic mouse models for NGCO by in vivo passaging of GEM tumors. These metastatic models provide a platform for evaluating new treatment strategies in preclinical studies aimed at improving outcomes in choriocarcinoma patients.

IL-12 overexpression in mice as a model for Sjögren lung disease

2006 ◽  
Vol 291 (4) ◽  
pp. L837-L846 ◽  
Author(s):  
Sharon McGrath-Morrow ◽  
Beth Laube ◽  
Shey-Cherng Tzou ◽  
Cecilia Cho ◽  
Jeffrey Cleary ◽  
...  
Keyword(s):  
Mouse Model ◽  
Nk Cells ◽  
Periodic Acid ◽  
Sjögren Syndrome ◽  
Lymphoid Cells ◽  
Interleukin 12 ◽  
Sjogren Syndrome ◽  
Wild Type ◽  
Periodic Acid Schiff ◽  
Lymphocytic Infiltrates

Interleukin-12 (IL-12), a Th1 proinflammatory cytokine, is reported to be increased in Sjögren syndrome. To evaluate the effects of local Th1/Th2 deregulation, we generated a transgenic mouse model that overexpresses IL-12 in the lungs. IL-12 transgenic mice developed bronchial and alveolar abnormalities strikingly similar to those found in the lungs of Sjögren patients. Pathologically, lung abnormalities began at ∼4 mo of age and were characterized by lymphocytic infiltrates around the bronchi, intraluminal periodic acid Schiff-positive debris, increased cell proliferation in the alveolar region, and increased interstitial and alveolar macrophages. Functionally, these abnormalities translated into decreased mucociliary clearance ( P < 0.05 vs. wild-type littermates) and increased oxidative stress ( P < 0.01). The pathological and functional abnormalities were accompanied by significant changes in lung natural killer (NK) cells. The number of NK cells was fourfold higher in IL-12 transgenic than wild-type lungs (20% of all lymphoid cells vs. 5%) during the first month of life. NK cells then decreased within a narrow window of time (from 30 to 50 days of age), reaching a nadir of ∼2% on day 50, and remained at these low levels thereafter. This new mouse model highlights the role of IL-12 in the initiation of Sjögren syndrome.

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