ABSTRACT
PURPOSE: This study aims to appraise the therapeutic effectiveness of intravitreal injections anti-vascular endothelial growth factor (anti-VEGF) vs alternative therapies in managing radiation retinopathy (RR). DESIGN: Systematic review and meta-analysis. METHODS: We obtained comprehensive data retrieval using PubMed, Embase, Web of Science, Scopus, and the Cochrane Library from their inception until December 15, 2023. This review included randomized controlled trials (RCTs) and nonrandomized studies (NRSs) reporting on best-corrected visual acuity (BCVA) among RR patients treated with intravitreal anti-VEGF. Study selection and data extraction were meticulously performed by 2 independent reviewers. The Cochrane Risk of Bias Tool 2.0 (RoB 2.0) and Risk of Bias in Nonrandomized Studies of Interventions (ROBINS-I) scales were utilized for bias risk assessment. Quantification of heterogeneity was executed using Q, H, and I2 statistics. The primary endpoint was the BCVA at the final observation point of each study. Secondary endpoints included central retinal thickness (CRT), foveal avascular zone (FAZ) area, and capillary density (CD) at the level of superficial capillary plexus. Subgroup analyses were undertaken to explore potential heterogeneity sources possibly due to treatment duration and study design. Sensitivity analyses were conducted to ascertain result stability. RESULTS: This analysis incorporated 7 studies (including 3 RCTs) encompassing 922 patients afflicted with RR. Relative to other treatment modalities, intravitreal anti-VEGF therapy was associated with a statistically significant mean decrease in BCVA of -0.34 logMAR (95% CI, -0.39 to -0.30 logMAR; I2 = 87.70%; P < .001), and a substantial reduction in CRT of -34.65 µm (95% CI, -50.70 to -18.60 µm; I2 = 30.40%; P < .001). Additionally, a reduction in the FAZ area by -0.69 mm² (95% CI, -0.91 to -0.46 mm², I2 = 0%; P < .001) was observed. A positive tendency was noted in CD at the superficial capillary plexus between anti-VEGF and other therapeutic interventions. CONCLUSIONS: Intravitreal anti-VEGF injections, in comparison to other treatments, demonstrate superior efficacy in enhancing BCVA and reducing CRT, thereby underscoring the potential of anti-VEGF in ameliorating radiation retinopathy outcomes. However, the conclusions are constrained by the incorporation of data from some NRSs and the small sample sizes.
Subject(s)
Angiogenesis Inhibitors , Intravitreal Injections , Radiation Injuries , Retinal Diseases , Vascular Endothelial Growth Factor A , Visual Acuity , Humans , Angiogenesis Inhibitors/therapeutic use , Angiogenesis Inhibitors/administration & dosage , Vascular Endothelial Growth Factor A/antagonists & inhibitors , Radiation Injuries/drug therapy , Visual Acuity/physiology , Retinal Diseases/drug therapy , Treatment Outcome , Tomography, Optical CoherenceABSTRACT
Plants rich in luteolin have been used as Chinese traditional medicines for inflammatory diseases, hypertension, and cancer. However, little is known about the effect of luteolin on the apoptosis or autophagy of the macrophages. In this study, mouse macrophage ANA-1 cells were incubated with different concentrations of luteolin. The viability of the cells was determined by an MTT assay, apoptosis was determined by flow cytometric analysis, the level of cell autophagy was observed by confocal microscopy, and the expression levels of apoptotic or autophagic and antiapoptotic or antiautophagic proteins were detected by Western blot analysis. The results showed that luteolin decreased the viability of ANA-1 cells and induced apoptosis and autophagy. Luteolin induced apoptosis accompanied by downregulation of the expression of Bcl-2 and upregulation of the expression of caspase 3 and caspase 8. And luteolin increased FITC-LC3 punctate fluorescence accompanied by the increased expression levels of LC3-I, ATG7, and ATG12, while it suppressed the expression level of Beclin-1. Luteolin treatment resulted in obvious activation of the p38, JNK, and Akt signaling pathways, which is important in modulating apoptosis and autophagy. Thus, we concluded that luteolin induced the apoptosis and autophagy of ANA-1 cells most likely by regulating the p38, JNK, and Akt pathways, inhibiting the activity of Bcl-2 and Beclin-1 and upregulating caspase 3 and caspase 8 expression. These results provide novel insights into a therapeutic strategy to prevent and possibly treat macrophage-related diseases through luteolin-induced apoptosis and autophagy.
Subject(s)
Luteolin/pharmacology , Macrophages/drug effects , Proto-Oncogene Proteins c-bcl-2/metabolism , Animals , Apoptosis , Autophagy , Caspase 3/metabolism , Caspase 8/metabolism , Cell Line , Flow Cytometry , Gene Expression Regulation , Macrophages/physiology , Medicine, Chinese Traditional , Mice , Microscopy, Confocal , Signal TransductionABSTRACT
OBJECTIVE: To compare the effect differences between auricular intradermal needling combined with erjian (HX6,7i) bloodletting and oral administration of western medicine, and to explore the efficacy of neuroendocrine level in patients with perimenopausal insomnia. METHODS: Ninety patients were randomized into an observation group and a control group, 45 cases in each one. In the observation group, auricular intradermal needling combined with erjian (HX6,7i) bloodletting were adopted alternately in the two ears. The auricular points were shen (CO10), xin (CO15), gan (CO12), shenmen (TF4), jiaogan (AH6a), neifenmi (CO18) and erjian (HX6,7i). The treatment was required once 3 days on the auricular points of one side alternatively. Oral administration of estazolam (1mg each day) was applied in the control group for 2 courses, 4 weeks as 1 course, once a day. The scores of Pittsburgh sleep quality index (PSQI), the levels of serum estrogen (E2), 5-hydroxy tryptamine (5-HT) and norepinephrine (NE) were valuated in the two groups before and after treatment. RESULTS: After treatment, the total scores of PSQI reduced in the two groups (both P<0.05), and the improvements of sleeping quality, sleeping time, sleeping difficulty, daytime dysfunction and the total PSQI score in the observation group were superior to those in the control group (all P<0.05). There was no significant difference in serum E2 before and after treatment in the two groupsï¼and between the two groups after treatment (all P>0.05). After treatment, 5-HT contents increased and NE levels decreased in the two groups (all P<0.05), with better results in the observation group (both P<0.05). The total effective rate was 95.6% (43/45) in the observation group, which was higher than 82.2% (37/45) in the control group (P<0.05). CONCLUSION: Auricular intradermal needling combined with erjian (HX6,7i) bloodletting can improve the sleep quality of patients with perimenopausal insomnia, and adjust the neurotransmitter level, which achieves better effect than western medication.
Subject(s)
Acupuncture Therapy , Sleep Initiation and Maintenance Disorders , Acupuncture Points , Bloodletting , Humans , Perimenopause , Sleep Initiation and Maintenance Disorders/therapy , Treatment OutcomeABSTRACT
OBJECTIVE: To study the regulation of luteolin on spleen cells and sarcoma S180 cells in normal ICR mice. METHODS: Spleen cells and S180 cells were incubated with different concentrations of luteolin (50, 100, 200, and 400 µmol/L). The effect of luteolin on spleen cells and sarcoma S180 cells was determined by MTT assay. The apoptosis was detected using propidium iodide staining flow cytometry. Intracellular reactive oxygen species (ROS) was determined by flow cytometric analysis. Activities of free radicals scavenging were determined by hydroxyl radical and DPPH tests. RESULTS: Compared with the solvent control group, 200 and 400 µmol/L luteolin increased the spleen cells viability (P < 0.05). Luteolin at 100, 200, and 400 µmol/L decreased activities of S180 cells (P < 0.01). The proportion of sub-G1 phase spleen cells was reduced after treated with 200 and 400 µmol/L luteolin (P < 0.05). The proportion of sub-G1 phase S180 cells was elevated after treated with 200 and 400 µmol/L luteolin (P < 0.05). Compared with the solvent control group, levels of intracellular ROS in spleen cells of ICR mice all increased; levels of intracellular ROS in S180 cells all decreased after treated with 50, 100, 200, and 400 µmol/L luteolin (P < 0.05). Luteolin scavenged hydroxyl radical and DPPH in a dose dependent manner. CONCLUSION: Luteolin had bilateral regulation on viability and apoptosis of spleen cells and S180 cells (promoting the viability of spleen cells, inhibiting apoptosis of spleen cells, inhibiting the viability of S180 cells, and promoting apoptosis of S180 cells), which was worth further study and exploration.