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Pterygium is an ocular surface disease formed by many factors and associate with a series of changes caused by ultraviolet irradiation and radiation, its pathogenesis is still uncertain. Elevated vascular endothelial growth factor(VEGF), inflammatory infiltrates, angiogenesis, oxidative stress, epithelial-mesenchymal cell transition(EMT), and tumor suppressor gene inactivation are currently recognized causes of pterygium. The mechanism of this factor in pterygium deveopment is still not completely understood. This review aimed to investigate the role of these factors in pterygium formation and provide targeted therapy and effective preventive measures for clinical diagnosis and treatment.
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The dry eye is a common ocular surface disease caused by multiple factors with multiple pathogenesis. With the increasing morbidity of dry eye in our country year by year, dry eye has gradually attracted people's attention. The pathogenesis of dry eye is more complicated whose critical influencing factors include inflammation, corneal and conjunctival epithelial cell changes, tear film composition changes, corneal nerve changes, and meibomian gland dysfunction and so on. The tear film hypertonicity leads to the hypertonicity of the ocular surface epithelial cells, stimulating the cascade of inflammation, which is the most critical part among the pathogenesis of dry eye. A variety of inflammatory mediators and immune cells are involved in this process, and more and more people have reached a consensus that the dry eye is an antigen-specific autoimmune inflammatory disease and they are closely correlated with each. In clinical treatment, various anti-inflammatory drugs and drugs promoting tear secretion mark the rapid development of drug therapy for dry eye to some extent, but dry eye treatment is not only to improve symptoms, but to carry out treatment according to specific etiology. Recently, researches on the immune mechanism of dry eye have been increasing. This article reviewed on the immune progress of dry eye to realize the clinical significance and systematically understand the role of which in the occurrence and development of dry eye.
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Up to now, a variety of microRNAs have been found in a number of studies, that specifically expressed in retinal neuroepithelial, lens, cornea and retinal pigment epithelium, in which miR-126 plays a certain role in the proliferation of tumor cells, the development of thymus lymphocytes and cardiovascular diseases.Some researches show that miR-126 has certain correlations with the formation of corneal neovascularization, the development of diabetic retinopathy, and the immune system related eye disease.In this paper, the current miR-126 in the role of eye disease mechanism and research progress were reviewed.
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<p><b>OBJECTIVE</b>To investigate the effect of total flavonoids of astragalus on the expression of endoplasmic reticulum chaperone, calumenin and connecxin 43 (CX43) in suckling mouse myocardium with myocarditis caused by coxsackievirus B3 (CVB3).</p><p><b>METHODS</b>The primary culture of suckling mouse myocardium cells were randomly divided into control group, CVB3 infected group and total flavonoids of astragalus group. Firstly, to confirm the identity of the suckling mouse myocardium, α-SMA was monitored by immunohistochemistry method. Then the protein expression changes of endoplasmic reticulum chaperone-glucose regulatory protein 78 ( GRP78), calumenin and CX43 were detected by Western blot.</p><p><b>RESULTS</b>(1) Compared with that of the control group, the GRP78 expression level in CVB3 infected group was improved, the expression levels of calumenin and CX43 were all reduced. (2) Compared with that of CVB3 infected group, GRP78 expression level was decreased, and the expression levels of calumenin and CX43 were increased in total flavonoids of astragalus group.</p><p><b>CONCLUSION</b>CVB3 infection may cause endoplasmic reticulum stress of rat myocardium cells by increasing the expression of GRP78 and decreasing the expression of calumenin and CX43. On the other hand, total flavonoids of astragalus can reduce the expression of GRP78 and increase the expression of calumenin and CX43.The results of this experiment may be closely related to the effects of anti-arrhythmia with viral myocarditis caused by CVB3.</p>
Subject(s)
Animals , Mice , Rats , Astragalus Plant , Chemistry , Blotting, Western , Calcium-Binding Proteins , Metabolism , Cells, Cultured , Connexin 43 , Metabolism , Coxsackievirus Infections , Drug Therapy , Endoplasmic Reticulum , Metabolism , Endoplasmic Reticulum Stress , Flavonoids , Pharmacology , Heat-Shock Proteins , Metabolism , Myocarditis , Drug Therapy , Virology , Myocardium , Cell Biology , Myocytes, Cardiac , VirologyABSTRACT
Background Corneal epithelial abrasion results in corneal ulcer and stroma cloudy evenb irreversible visual impairment.Previous drugs for corneal epithelial injury can only alleviate the inflammatory irritation.So it is very important to seek a drug which regulate the growth of corneal epithelium.Objective This study was to investigate the effects of recombinant human BIGH3 protein eye drops on corneal epithelial abrasion.Methods Fifty right eyes of 50 clean adult New Zealand white rabbits were collected.Two rabbits were sacrificed right away following establishment of corneal epithelial abrasion models (0 hour group).The other 48 rabbits were randomly divided into recombinant human epidermal growth factor (EGF) derivative group (positive control group),normal saline solution group (negative control group),0.25％ or 0.5％ recombinant human BIGH3 protein eye drops group.Corneal abrasion models were created with alcohol corrosion method with a defect area of 7 mm2.The corresponding eye drops were used separately in 4 groups for four times per day after operation.Experimental eyes were examined by the slit lamp microscope,and fluorescein vital staining were performed 12,24,36,48,72 hours after operation.Planimetry was performed and the corneal photographs were analyzed with computer software.The rabbits were sacrificed 12,24,36,48 and 72 hours after operation,respectively,and the histopathological examination of corneal tissue was carried out.Results No obvious irritation response was seen after administered of eye drops in the recombinant human EGF derivative group,normal saline solution group,0.25％ and 0.5％ recombinant human BIGH3 protein eye drops groups.Histopathological examination revealed a full-thickness defect of corneal epithelium after modeling.The defect area was gradually smaller with time lapse,and corneal epithelium migrated from periphery toward the center zone.Corneal epithelial cells increased with time lapse.Compared with normal saline solution group,the defect area of corneal epithelium lessened 12,24,36,48 hours after operation in the 0.25％,0.5％ recombinant human BIGH3 protein eye drops groups and recombinant human EGF derivative group (all at P =0.000),but at 12and 24,36 hours after operation,no significant differences were found between the recombinant human EGF derivative group and normal saline solution group (P =0.321,0.057,0.126).The defect area was smaller in the 0.5％recombinant human BIGH3 protein eye drops group than that of the recombinant human EGF derivative group at various time points (P=0.042,0.039,0.025,0.008).However,significant smaller defect area was exhibited only at 12 hours and 24 hours after operation in the 0.25％ recombinant human BIGH3 protein eye drops group (P=0.047,0.042).No significant differences were seen in corneal defect area at various time points between 0.25％ and 0.5％recombinant human BIGH3 protein eye drops groups (P =0.358,0.259,0.108,0.062).In addition,the corneal defect area was (0.51 ±0.42)mm2 72 hours after operation in the normal saline group;while that in the recombinant human EGF derivative group and recombinant human BIGH3 protein eye drops groups was disappeared.The repairing curves in the recombinant human BIGH3 protein eye drops groups were superior to those of the recombinant human EGF derivative group and normal saline solution group.Conclusions 0.25％ and 0.5％ recombinant human BIGH3 protein eye drops have facilitation effect on the growth of corneal epithelial cells and the healing of corneal injury.
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Background Interleukin-17 (IL-17)is a potent pro-inflammatory cytokine and plays a pathogenic role in autoimmune disease.It was confirmed that IL-17 is implicated in allograft rejection of many transplanted organs.Recent studies have foensed on the effect of IL-17 antagonists on allograft rejection.Objective This study aimed to investigate the inhibitory effect of anti-mouse IL-17 monoclonal antibody (mAb) on corneal allograft rejection.Methods Twenty-five 8 to 10-week-old C57BL/6 mice and 50 BALB/c mice were collected.Donor cornea grafts with 2 mm diameter from 25 C57BL/6 mice was transplanted to 50 eye of BALB/c mice to establish a model of corneal transplantation.The recipients were randomized into 2 groups,and neutralizing mouse IL-17antibody or isotype control antibody was intraperitoneally injected immediately after transplantation for experimental treatment,respectively.Allografts were scored clinically at appropriate time points after treatment based on Plskova criteria,and ≥5 was confirmed as rejection.Infiltrating cells in corneal graft were detected qualitatively and quantitatively by immunohistochemistry and reverse transcription-PCR separately.The cytokine levels of T helper type 1 (Th1),Th2,and Th17 in recipients' spleen wer(c) analyzcd by ELISA.The use of the animals followed the Statement of ARVO.Results Compared with the isotype control antibody group,the survival of grafts was improved in the IL-17mAb group(P＜0.05).The levels of neutrophile granulocyte mRNA,CD4+ and CD8+ T lymphotes mRNA were 2.22±0.10,1.64±0.04 and 1.32±0.10 in the IL-17 mAb group,showing a significant decline in comparison with those of the isotype control antibody group(3.61 ±0.08,2.69±0.06 and 2.17±0.04) (P=0.000,0.000,0.000).Interferon-γ(IFN-γ),IL-12 p40 and IL-17 concentrations in recipients ' splenocytes were (529.80 ± 13.83) ng/L,(539.58 ±10.74) ng/L and(173.70±8.11)ng/L in the IL-17 mAb group,and thosc in the isotype control antibody group were (741.48± 10.51) ng/L,(1156.90 ± 69.93) ng/L and (366.13± 7.93) ng/L,with significant differences between them (P=0.000,0.001,0.000).Conclusions Neutralization IL-17 bioactivity inhibits mouse corneal allograft rejection to a certain extent.
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BackgroundEndostatin (ES) is currently the strongest endogenous angiognesis inhibitor,and it can inhibit the occurrence of neovascularization.Various studies demonstrated that the poly RGD sequence can enhance the function of the ES gene.ObjectiveThis study was to evaluate the use of gene therapy of modified ES for alkaline burn-induced corneal neovascularization (CNV).MethodsOne hundred and two clean SD rats were randomly divided into the normal control group,the pCI empty vector group,the pCI-ES group,and the pCI-RGDRGDES group.Corneal neovascularization models were established by placing a piece of 3 mm filter paper with 1 mol/L NaOH at the central cornea for 40 seconds.3 μg of the pCI blank vector,ES-tranfected pCI blank vector,or RGDRGD-ES-transfected pCI vector was injected into the superior bulbar conjunctiva after the alkali burn twice at 1-week intervals.Area of CNV and edema of the cornea in the various groups of rats were examined daily under the slit lamp biomicroscope.1,4,7 and 14 days after operation,the rats were sacrificed by the excessive anesthesia method and corneal tissues were obtained to evaluate pathological changes.The expression of CD34 in vascular endothelial cells was detected by immunochemistry to calculate the corneal neovascular density.The expressions of VEGF mRNA and Flk-1 protein in the corneas were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.The use and maintenance of animals followed the Statement of ARVO.Results Seven to fourteen days after corneal alkali-burning,the corneal neovascular area was smaller in the pCI-ES group and pCI-RGDRGD-ES group compared with the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and nevascular area in the pCI-RGDRGD-ES group was smaller than that in the pCI-ES group (P＜0.05).The expression level of CD34 was significantly lower in the pCI-ES group and pCI-RGDRGD-ES group than that in the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and the expression level of CD34 was further declined in the pCI-RGDRGD-ES group compared with the pCI-ES group (P＜0.05 ).Compared with the normal control group and pCI vector group,the expressions of the Flk-1 protein and VEGF mRNA were decreased in the pCI-ES group and pCI-RGDRGD-ES group on the fourth day after corneal alkali-burning (P＜0.01,P＜0.05 ),and those in the pCI-RGDRGD-ES group were less than the pCI-ES group (P＜ 0.05,P＜ 0.05 ).Conclusions Subconjunctival injection of both ES and modified RGDRGD-ES genes result in significant suppression of CNV in vivo,and modified RGDRGD-ES appears to be more effective than native ES.The main mechanism of ES in inhibiting neovascularization is to downregulate the expression of VEGF and Flk-1.
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<p><b>OBJECTIVE</b>To explore a better therapeutic method for acute pancreatitis.</p><p><b>METHODS</b>Sixty-three cases of acute pancreatitis were randomly divided into an observation group (31 cases) and a control group (32 cases). In the control group, routine treatment of western medicine included fasting, gastric acid and trypsinase secretion inhibition were applied, while acupoint application was added in the observation group. Yishu (Extra), Zhongwan (CV 12), Neiguan (PC 6), Zusanli (ST 36) and Pishu (BL 20) were selected as the main acupoints. The magnetic plaster was applied to the acupoints mentioned and changed once per day. Seven days made one session.</p><p><b>RESULTS</b>The cured rate in the observation group was 90.3% (28/31), which was significantly higher than that of 71.9%, (23/32) in the control group (P < 0.05). The recovery time of hyper-serum amylase, hyper-uric amylase and hyper-leukocytes in the observation group was significantly shorter than that in the control group [(3.5 +/- 0.9) days vs (5.9 +/- 0.8) days, (6.1 +/- 1.5) days vs (10.5 +/- 1.8) days, (6.8 +/- 1.4) days vs (9.7 +/- 1.6) days, all P < 0.05]. The hospital stays and expenses in the observation group were significantly lower than those in the control group [(7.9 +/- 0.9) days vs (11.7 +/- 1.4) days, (5.3 +/- 1.1) thousand RMB vs (8.9 +/- 1.5) thousand RMB, both P < 0.05].</p><p><b>CONCLUSION</b>Acupoint application combined with routine treatment of western medicine is effective and can be considered as a better therapy for acute pancreatitis.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Acupuncture Points , Acupuncture Therapy , Methods , Acute Disease , Combined Modality Therapy , Medicine, Chinese Traditional , Pancreatitis , TherapeuticsABSTRACT
Background Oxidative stress is thought to be responsible to diabetes-complicated cataract.Our previous study demonstrated that as an iron chelator,deferiprone can protect lens from oxidative damage.Objective This further study aimed to investigate the role of deferiprone on the formation of diabetic-complicated cataract.Methods Forty 6-week-old Wistar rats were included in the study and randomized into 4 groups.Eight of them were used as the normal control group.Diabetes mellitus animal models were established in 22 rats by the carbonhydratediet and fat diet and the intraperitoneal injection of 40 mg/kg streptozocin (STZ).The deferiprone of 50 mg and 100 mg were intragastrically given in 8 model rats respectively after 3 days once a day for 8 weeks.The opacification of lenses was examined under the slit lamp weekly after treatment.The animals were sacrificed and the lenses were obtained at the eighth week of deferiprone injection.The concentrations of water-soluble protein ( WSP),urine-soluble protein (USP) and alkali-soluble protein (ASP) in rat lens suspension were detected by Bradford method.The super oxide dimutese (SOD),malondialdehyde (MDA) and glutathione (GSH) were determined spectrometically using xanthine oxidase,thiobarbituric acid,dithio bis-nitrobenzoic acid.Results No evidently differences were found in the content of the WSP,USP and ASP among the these groups( F=1.73,0.18,0.09,P＞0.05).The contents of MDA in 50 mg deferiprone group and 100 mg deferiprone group were ( 1.05 ± 0.10 ) mmol/g and ( 1.05 ± 0.22 ) mmol/g respectively,showing a significant decline in comparison with diabetic model group (P＜0.05).The SOD and GSH contents in lens were (321.29±16.57) U/mg,(322.07±22.16) U/mg and (7.83±0.65 ) mg/g,(7.70±0.77 ) mg/g respectively in 50 mg deferiprone group and 100 mg deferiprone group and were considerably elevated in comparison with ( 298.70± 14.69 ) U/mg and ( 5.47 ± 1.01 ) mg/g of diabetic model groups ( P＜0.05 ).No significant differences were found in the indexes mentioned above between 50 mg and 100 mg deferiprone groups(P＞0.05).Conclusions Deferiprone can reduce oxidative stress and improve the energy metabolism of the lens in diabetic rats.
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Background Researches demonstrated that the long-term application of glucocorticoids can induce cataract. However, its molecular mechanism is unclear. Objective Present study was to investigate the effects of dexamethasone on the regulation of nuclear factor kappa B( NF-κB)/ inhibitor kappa B alpha( IκBα) line on human lens epithelial cells (LECs) and the LECs apoptosis. Methods Human LECs line(HLE2B3) were cultured and passaged in DMEM containing 20% fetal bovine serum and treated by different concentrations of dexamethasone(0. 01,0. 1,1,10,100 μmol/L) for 24,36 and 48 hours respectively. The LECs cultured in free-serum DMEM without dexamethasone were as blank control group. The expressions of IκBo: in the LECs were examined by reverse transcription polymerase chain reaction ( RT-PCR) and Western blot, and the expressions of NF-κB neucleoprotein in LECs were detected by Western blot after exposure to dexamethasone. The apoptosis rate of LECs was determined by flow cytometer. Results Agarose gel electrophoresis showed that the amplified gene fragment was coincident to designed one. The expressing level of NF-κB neucleoprotein in LECs was significantly lowed with the increase of dexamethasone concentration ( F = 36. 077 , P = 0. 004 ) , and that of IkBo: was evidently ascended ( F = 35. 741 ,P = 0. 002). In the same concentration of dexamethasone group,the expression of NF-κB in LECs showed the considerable alteration in different duration after treated of dexamethasone with the lowest expressing level in 36 hours, and significant differences were found in the expressing level between 24 hours and 36 hours ( P = 0. 002) and between 24 hours and 48 hours (P = 0. 01). The differences of expression of IκBá in LECs appeared the same pattern to NF-κB neucleoprotein. Flow cytometry showed that the apoptosis rate of LECs was obviously enhanced after action of dexamethasone in a dose-dependent manner, showing a significant difference among different groups ( F = 73. 261, P = 0.001). Conclusion It is implied that dexamethasone results in the pathogenesis and development of glucocorticoid cataract by up-regulating the expression of IκBα in LECs and suppressing the activity of NF-κB and herein induce the apoptosis of LECs at concentration-and time-dependent manner. This might be one of cellular and biological mechanisms of glucocorticoid cataract formation.
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Background RGD is a small molecular multiple peptide containing Arg-Gly-Asp with an important role in inhibiting the adhesion,migration and neovascularization of tumor.Our previous study determined that RGD can suppress the adhesion and proliferation of lens epithelial cells(LECs),and RGDRGD may be of a stronger effect. Objective Present study was to investigate and compare the effect of RGDRGD peptide on the proliferation and adhesion of immortalized human LECs(HLEB-3)in vitro. Methods Human LECs harvested by trpsin-EDTA were suspended in DMEM medium with serial dilutions of RGD peptide and RGDRGD peptide(from 1000 mg/L to 250 mg/L)at 37℃ for 15 minutes as experimental group,and the HLECs cultured by common culture medium were used as the control group.The cells were then seeded into the 96-well plates with precoated fibmnectin (FN)and I collagen at the density of 2×104/ml.MTT stainingcolorimetry was used to measure the adhesion rates of lens epithelial cells cultured in different concentrations RGDRGD and RGD peptides after 1 hour.Cells were seeded into the 96-well plates for 24 hours at 37℃ in 5% CO2.Medium was then replaced with DMEM overnight.Subsequently,the cells were treated with serial dilutions of RGD and RGDRGD(from 2000 mg/L to 250 ms/L)dissolved in DMEM medium plus 20% fetal bovine serum.The inhibition of RGDRGD and RGD on the adhesion and proliferation of Human LECs was analyzed by MTT aher 24,48 and 72 hours. Results The inhibition rate of RGD peptide on the adhesion of LECs was gradually enhanced with the increase of concentration with the significant difference among the different concentrations groups(F=1089.56,P＜0.01),and the statistically significant elevation in inhibitory rate was found in RGDRGD peptide compared with RGD peptide(P＜0.01).The inhibition rate of RGDRGD peptide on the proliferation of LECs wag gradually increased with the increase of concentration with the significant difference among the different concentrations groups with a strongest effect in 1000 ms/L group(F=127.31,P＜0.01),and the much stronger inhibition Wag Been in RGDRGD peptide(F=1589.85,P＜0.01).The suppression rate of RGDRGD on LECs proliferation Wag much stronger with the prolong of time(F=1606.43,P＜0.01). Conclusion RGDRGD peptide and RGD peptide have inhibitory effect on adhesion and proliferation of human LECs in a dose-and time-dependent manner.Effect of RGDRGD peptide is much stronger than RGD peptide.These results imply that RGDRGD peptide and RGD peptide have the important role for prevention of PCO.
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Endostatin(ES), the C-terminal fragment of collagen XVIII, is a potent angiogenesis inhibitor. At present, there are a large number of research papers on ES. It has already been on clinical stage Ⅱ and been widely used in inhibition of neovascularization(NV). However, how to improve the bioactivity of ES is still a matter of ongoing discussion. The objective of this review is to elucidate the relationship between the modified ES and ocular neovascualrization, and to discuss the superiority based on the structure modification. The structure can be changed either by covalent modification or by genetical mutation. It is proposed that the secondary structral ES enhance the anti-angiogenic activity. Studies on modified ES also shed light on our understanding of the molecular action mechanisms of ES. Modified ES may be exploited as a new angiogenesis inhibitor for therapeutic applica-tions, in substitution of the native ES. Activity
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<p><b>OBJECTIVE</b>To observe the effect of acupuncture on gastrointestinal responses after renal transplantation.</p><p><b>METHODS</b>Sixty cases with gastrointestinal responses after renal transplantation were randomly divided into an acupuncture group and a medication group, 30 cases in each group. The acupuncture group were treated with acupuncture at Neiguan (PC 6), Zusanli (ST 36), Sanyinjiao (SP 6), etc.; the medication group were treated with oral administration of Weilexin. The symptoms of abdominal pain, nausea, gastric distention, and other gastrointestinal responses were observed in the two groups.</p><p><b>RESULTS</b>The effective rate was 93.3% in the acupuncture group and 76.7% in the medication group with a very significant difference between the two groups (P < 0.01), the acupuncture group being significantly better than the medication group.</p><p><b>CONCLUSION</b>Acupuncture has a good effect of promoting recovery of gastrointestinal function after renal transplantation.</p>