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AIM: To compare the efficacy of and without small incision lenticule extraction(SMILE)with cyclotorsion compensation for astigmatism correction.METHODS: PubMed, Web of Science, EMBASE, Cochrane and CNKI, VIP, CBM, and Wan Fang Data were searched for clinically controlled studies from January 2010 to August 2022, including an experimental group with cyclotorsion compensation during SMILE and a control group without cyclotorsion compensation during SMILE. After literature screening, quality evaluation, and data extraction by two researchers independently, the Meta-analysis of uncorrected distance visual acuity(UDVA), residual astigmatism, vector analysis indicators for measuring the astigmatism correction including absolute value of angle of error(|AE|)and magnitude error(ME), and post-operative total higher order aberrations, spherical aberration and coma was carried out with Stata 16.0 software.RESULTS: Seven studies with a total of 846 eyes(442 in the experimental group, 404 in the control group)were finally included. The Meta-analysis showed that there were significant differences in the percentage of eyes with residual astigmatism ≥1.00D(OR=0.17, 95%CI: 0.06~0.49, P<0.01), |AE|(WMD=-1.56, 95%CI: -2.68~-0.45, P<0.01), the coma(WMD=0.06, 95%CI: -0.08~-0.04, P<0.01), and the total higher order aberrations(WMD=-0.04, 95%CI: -0.06~-0.02, P<0.01). However, there were no differences in the postoperative UDVA(WMD=0.00, 95%CI: -0.02~0.01, P=0.54), residual astigmatism(WMD=0.08, 95%CI: -0.02~0.18, P=0.10), ME(WMD=-0.01, 95%CI: -0.14~0.12, P=0.85), and the spherical aberration(WMD=0.03, 95%CI: -0.07~0.13, P=0.52).CONCLUSION: Cyclotorsion compensation in SMILE can reduce the angular error caused by eye rotation during astigmatism correction. It also decreases postoperative residual astigmatism. Overall, the SMILE with cyclotorsion compensation is superior in clinical efficacy of the precise correction of astigmatism.
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AIM: To compare the changes in corneal densitometry after small incision lenticule extraction(SMILE)and femtosecond laser in situ keratomileusis(FS-LASIK)and investigate the effect of corneal interface haze on vision after SMILE.METHODS: Prospective cohort study. A total of 93 patients(186 eyes)who were scheduled to undergo refractive surgery at the Ophthalmic Refractive Surgery Center of the Affiliated Hospital of Nantong University from May 2020 to October 2021 were included in the study, and there were 48 patients(96 eyes)in the SMILE group and 45 patients(90 eyes)in the FS-LASIK group. The changes in corneal densitometry, spherical equivalent(SE), and uncorrected visual acuity(UCVA)were observed and compared between the two groups before and at 1d, 1wk, 1, 3 and 6mo after surgery.RESULTS: The 93 patients all successfully completed the surgery, and there were no related complications during and after the surgery, and there were no lost cases. The UCVA of FS-LASIK group was 0.044±0.064 and -0.001±0.065 respectively at 1d and 1wk after surgery, which was better than that of SMILE group(0.102±0.077 and 0.023±0.064; all P<0.05). There was no statistical difference in the SE between the two groups at the postoperative follow-ups(P>0.05). The corneal densitometry values at 0-2 and 2-6 mm from corneal vertex and total corneal densitometry at 1d postoperatively in the FS-LASIK group were 18.0(17.5, 18.6), 16.2(15.6, 16.7)and 16.7(16.1, 17.3), which were lower than those of SMILE group [18.6(18.1, 19.3), 16.8(16.4, 17.4), 17.2(16.6, 17.8)](all P<0.05); The corneal densitometry values at 0-2 and 2-6 mm from corneal vertex and total corneal densitometry at 1wk postoperatively in the FS-LASIK group were 17.2(16.7, 17.6), 15.5(15.0, 15.9)and 15.9(15.3, 16.7), which were lower than those of SMILE group [17.6(17.1, 18.3), 16.0(15.6, 16.5), 16.6(15.9, 17.1)](all P<0.05).CONCLUSIONS: The transient interface haze after SMILE is responsible for the early higher corneal densitometry than FS-LASIK. The presence of interface haze is probably a factor for the quality of vision.
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The aim of this study is to explore the mechanism of ligustilide, the main active constituent of essential oils of traditional Chinese medicine Angelicae Sinensis Radix, on alleviating oxygen-glucose deprivation/reperfusion(OGD/R) injury in PC12 cells from the perspective of ferroptosis. OGD/R was induced in vitro, and 12 h after ligustilide addition during reperfusion, cell viability was detected by cell counting kit-8(CCK-8) assay. DCFH-DA staining was used to detect the level of intracellular reactive oxygen species(ROS). Western blot was employed to detect the expression of ferroptosis-related proteins, glutathione peroxidase 4(GPX4), transferrin receptor 1(TFR1), and solute carrier family 7 member 11(SLC7A11), and ferritinophagy-related proteins, nuclear receptor coactivator 4(NCOA4), ferritin heavy chain 1(FTH1), and microtubule-associated protein 1 light chain 3(LC3). The fluorescence intensity of LC3 protein was analyzed by immunofluorescence staining. The content of glutathione(GSH), malondialdehyde(MDA), and Fe was detected by chemiluminescent immunoassay. The effect of ligustilide on ferroptosis was observed by overexpression of NCOA4 gene. The results showed that ligustilide increased the viability of PC12 cells damaged by OGD/R, inhibited the release of ROS, reduced the content of Fe and MDA and the expression of TFR1, NCOA4, and LC3, and improved the content of GSH and the expression of GPX4, SLC7A11, and FTH1 compared with OGD/R group. After overexpression of the key protein NCOA4 in ferritinophagy, the inhibitory effect of ligustilide on ferroptosis was partially reversed, indicating that ligustilide may alleviate OGD/R injury of PC12 cells by blocking ferritinophagy and then inhibiting ferroptosis. The mechanism by which ligustilide reduced OGD/R injury in PC12 cells is that it suppressed the ferroptosis involved in ferritinophagy.
الموضوعات
Animals , Rats , PC12 Cells , Ferroptosis/genetics , Reactive Oxygen Species , Transcription Factors , Glutathioneالملخص
Pentaxin 3 (PTX3), as a multifunctional glycoprotein, plays an important role in regulating inflammatory response, promoting tissue repair, inducing ectopic calcification and maintaining bone homeostasis. The effect of PTX3 on bone mineral density (BMD) may be affected by many factors. In PTX3 knockout mice and osteoporosis (OP) patients, the deletion of PTX3 will lead to decrease of BMD. In Korean community "Dong-gu study", it was found that plasma PTX3 was negatively correlated with BMD of femoral neck in male elderly patients. In terms of bone related cells, PTX3 plays an important role in maintaining the phenotype and function of osteoblasts (OB) in OP state;for osteoclast (OC), PTX3 in inflammatory state could stimulate nuclear factor κ receptor activator of nuclear factor-κB ligand (RANKL) production and its combination with TNF-stimulated gene 6(TSG-6) could improve activity of osteoclasts and promote bone resorption;for mesenchymal stem cells (MSCs), PTX3 could promote osteogenic differentiation of MSCs through PI3K/Akt signaling pathway. In recent years, the role of PTX3 as a new bone metabolism regulator in OP and fracture healing has been gradually concerned by scholars. In OP patients, PTX3 regulates bone mass mainly by promoting bone regeneration. In the process of fracture healing, PTX3 promotes fracture healing by coordinating bone regeneration and bone resorption to maintain bone homeostasis. In view of the above biological characteristics, PTX3 is expected to become a new target for the diagnosis and treatment of OP and other age-related bone diseases and fracture healing.
الموضوعات
Animals , Male , Mice , Bone Resorption/metabolism , Cell Differentiation , Fracture Healing/genetics , Osteoblasts , Osteoclasts , Osteogenesis , Osteoporosis/genetics , Phosphatidylinositol 3-Kinases/pharmacologyالملخص
This study explores the effect of total flavonoids of Rhododendra simsii(TFR) on middle cerebral artery occlusion(MCAO)-induced cerebral injury in rats and oxygen-glucose deprivation/reoxygenation(OGD/R) injury in PC12 cells and the underlying mechanism. The MCAO method was used to induce focal ischemic cerebral injury in rats. Male SD rats were randomized into sham group, model group, and TFR group. After MCAO, TFR(60 mg·kg~(-1)) was administered for 3 days. The content of tumor necrosis factor-α(TNF-α), interleukin-1(IL-1), and interleukin-6(IL-6) in serum was detected by enzyme-linked immunosorbent assay(ELISA). The pathological changes of brain tissue and cerebral infarction were observed based on hematoxylin and eosin(HE) staining and 2,3,5-triphenyltetrazolium chloride(TTC) staining. RT-qPCR and Western blot were used to detect the mRNA and protein levels of calcium release-activated calcium channel modulator 1(ORAI1), stromal interaction molecule 1(STIM1), stromal intera-ction molecule 2(STIM2), protein kinase B(PKB), and cysteinyl aspartate specific proteinase 3(caspase-3) in brain tissues. The OGD/R method was employed to induce injury in PC12 cells. Cells were randomized into the normal group, model group, gene silencing group, TFR(30 μg·mL~(-1)) group, and TFR(30 μg·mL~(-1))+gene overexpression plasmid group. Intracellular Ca~(2+) concentration and apoptosis rate of PC12 cells were measured by laser scanning confocal microscopy and flow cytometry. The effect of STIM-ORAI-regulated store-operated calcium entry(SOCE) pathway on TFR was explored based on gene silencing and gene overexpression techniques. The results showed that TFR significantly alleviated the histopathological damage of brains in MCAO rats after 3 days of admini-stration, reduced the contents of TNF-α, IL-1, and IL-6 in the serum, down-regulated the expression of ORAI1, STIM1, STIM2, and caspase-3 genes, and up-regulated the expression of PKB gene in brain tissues of MCAO rats. TFR significantly decreased OGD/R induced Ca~(2+) overload and apoptosis in PC12 cells. However, it induced TFR-like effect by ORAI1, STIM1 and STIM2 genes silencing. However, overexpression of these genes significantly blocked the effect of TFR in reducing Ca~(2+) overload and apoptosis in PC12 cells. In summary, in the early stage of focal cerebral ischemia-reperfusion injury and OGD/R-induced injury in PC12 cells TFR attenuates ischemic brain injury by inhibiting the STIM-ORAI-regulated SOCE pathway and reducing Ca~(2+) overload and inflammatory factor expression, and apoptosis.
الموضوعات
Animals , Male , Rats , Apoptosis , Brain Ischemia/metabolism , Caspase 3 , Interleukin-1 , Interleukin-6 , Rats, Sprague-Dawley , Reperfusion Injury/metabolism , Tumor Necrosis Factor-alpha/genetics , Flavonoids/pharmacology , Rhododendron/chemistryالملخص
OBJECTIVE To explore the effect of total flavonoids of Rhododendra simsii (TFR) on improving cerebral ischemia/reperfusion injury (CIRI) and its relationship with STIM/Orai-regulated operational Ca2+influx (SOCE) pathway. METHODS Oxygen-glucose deprivation/reoxygenation (OGD/R) PC12 cells were used to simulate CIRI in vitro, and the intracellular Ca2+ concentration and apoptosis rate of PC12 cells were detected by laser confocal microscope and flow cytometry, respectively. The regulation of STIM/Orai on SOCE was analyzed by STIM/Orai gene silencing and STIM/Orai gene overexpression. The CIRI model was established by MCAO in SD rats. The activities of inflammatory cyto?kines IL-1, IL-6 and TNF-αin serum were detected by ELISA. The pathological changes of ischemic brain tissue and the infarction of rat brain tissue were detected by HE staining and TTC staining. The protein and mRNA expression levels of STIM1, STIM2, Orai1, caspase-3 and PKB in brain tissue were detected by Western blotting and RT-qPCR, respectively. RESULTS The results of in vitro experiment showed that the fluorescence intensity of Ca2+ and apoptosis rate in PC12 cells treated with TFR were significantly lower than those in OGD/R group, and this trend was enhanced by SOCE antagonist 2-APB. STIM1/STIM2/Orai1 gene silencing significantly reduced apoptosis and Ca2+overload in OGD/R model, while TFR combined with overexpression of STIM1/STIM2/Orai1 aggravated apoptosis and Ca2+overload. In the in vivo experiment, TFR significantly reduced the brain histopathological damage, infarction of brain tissue, the contents of IL-1, IL-6 and TNF-α in the serum in MCAO rats and down-regulated the expression of STIM1, STIM2, Orai1 and caspase-3 protein and mRNA in the brain tissue, and up-regulated the expression of PKB. The above effects were enhanced by the addition of 2-APB. CONCLUSION The above results indicate that TFR may reduce the contents of inflammatory factors and apoptosis, decrease Ca2+ overload and ameliorate brain injury by inhibiting SOCE pathway mediated by STIM and Orai, suggesting that it has a protective effect against subacute CIRI.
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OBJECTIVE To predict the potential targets of hyperoside (Hyp) on improving ischemia/reperfusion injury by network pharmacology, and explore its possible mechanism combined with related literature. METHODS The action targets of Hyp and ischemia/reperfusion injury were obtained by TCMSP, Swiss Target Prediction, Pharm Mapper, Simi?larity ensemble approach, Online Mendelian Inheritance in Man, DisGENT and database. The common targets of drugs and diseases were screened by Omishare and STRING database respectively, and the protein-protein interaction (PPI) network map was constructed. Then the interaction network between Hyp and disease targets was constructed by Cyto?scape software and topological cross-linking analysis was carried out. Then the interaction network between Hyp and disease targets was constructed and cross-linked analysis was carried out by using Cytoscape software. The gene ontol?ogy (GO) of the core target was analyzed by David database, and then the related pathways of the core target were enriched by KEGG database. RESULTS A total of 54 GO enrichment processes were obtained by GO enrichment anal?ysis of 44 common genes, including 38 biological processes (BP), 15 cell composition (CC) processes, and 1 molecular functional (MF) process. 43 items were obtained by signal pathway enrichment analysis in KEGG database. CONCLU?SION It is suggested that the mechanism of Hyp may be related to PI3K-Akt, RAP1, RAS, VEGF and other signal trans?duction pathways. The above results laid a theoretical foundation for the study of the mechanism and clinical application of the treatment of ischemia/reperfusion injury.
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OBJECTIVE: To explore the clinical value of three-dimensional visualization technology in the resection of retroperitoneal tumor.METHODS: A retrospective analysis was performed on 91 patients with retroperitoneal tumor who underwent surgical resection in Department of General Surgery,Affiliated Sixth People's Hospital of Shanghai Jiao Tong University from January 2014 to December 2018.The three-dimensional visualization technology was used to observe the relationship between retroperitoneal tumors and surrounding tissues and blood vessels,to assess the resectability of the tumor and guide the development of the surgical plan.RESULTS: The median operation time was 178 minutes,the median blood loss was 543 mL,and the average tumor size was 12.8 cm.Nine cases(9.9%) were with postoperative complications and 1 died of seizures,82 patients with pathological examination of tumor capsule integrity,and the rate of complete resection is 90%.CONCLUSION: Preoperative application of three-dimensional visualization technique in the resection of retroperitoneal tumor can improve preoperative assessment accuracy and guide the formulation of individualized precision surgical procedures,meanwhile,to enable patients to achieve better surgical results.
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· Endoplasmic reticulum (ER) is a place where it folds and synthesizes the proteins.ER stress was induced when a variety of physiological and pathological factors happened,under which the protein misfolding occurred,the unfolded protein accumulated and the calcium ion imbalanced in the ER.The ER of high-glucose environment can change the protein redox state and produce reactive oxygen species,which affects the ER channel function and chaperone protein buffer;meanwhile changes the balance of calcium ions;finally induces the formation of ER stress.More and more studies have confirmed that ER stress in high glucose environment can cause a variety of ophthalmic diseases.So we review the recent articles about ER stress of high glucose environment and its related ophthalmic diseases.
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Corneal endothelial cell(CEC)is the most critical part for the cornea, of which activity can influence the postoperative vision.It is very important for the clinical cornea preservation considering the function and its self-purification of donor cornea.There are a variety of classical methods, which can significantly prolong the saving time of donor cornea with its good quality of CEC.We reviewed the published papers about present preservation methods of cornea, which can give us many suggestions for the clinical cornea preservation.