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Background: Endometriosis is a common and complex syndrome characterized by the presence of endometrial-like tissue outside the uterus. Chinese medicine has been recently found to show good efficacy in treating endometriosis. Our previous results revealed that Maqian fruit essential oil (MQEO) could inhibit the proliferation and induce apoptosis of ectopic endometrial stromal cells (EESCs), but the mechanisms remain unclear. In this study, we aim to explore the molecular mechanism of MQEO's specific effects in EESCs. Methods: We conducted a quantitative proteomics analysis by iTRAQ on EESCs treated with MQEO or DMSO. Then deep analysis was performed based on differentially expressed proteins, including Gene Ontology enrichment analysis, pathway enrichment analysis and protein interaction analysis. Candidate protein targets were subsequently verified by western blotting. Results: Among 6575 identified proteins, 435 proteins exhibited altered expression levels in MQEO-treated EESCs. Of these proteins, most were distributed in signal transduction as well as immune system and the most significantly altered pathway was complement and coagulation cascades. Moreover, two differentially expressed proteins (Heme oxygenase 1 and Acyl-CoA 6-desaturase) were verified and they can be potential biomarkers for endometriosis treatment. Conclusions: Our proteomic analysis revealed distinct protein expression patterns induced by MQEO treatment in EESCs, highlighting the potential of MQEO for endometriosis treatment and biomarker discovery. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy (DR) is a sight-threatening complication of diabetes. This study investigated the therapeutic effect of probucol in a mouse model of diabetic retinopathy. C57BL/6 mice were rendered diabetic through Streptozotocin (STZ) intraperitoneal injection. Mice were treated with probucol (150 mg/kg, gavage administration) or vehicle (DMSO) for 12 weeks. Optical coherence tomography (OCT), fundus photography (FP), and fundus fluorescein angiography (FFA) were conducted to evaluate retinal structure and damage. Eyes were collected for histology, reactive oxygen species (ROS) assay, apoptotic cells count, and western blot. After STZ injection, all mice developed hyperglycemia. Compared with the retina of the control group, the retina of diabetic mice showed enhanced arterial reflex and beaded vein dilatation. Besides, reduced inner and middle retinal thickness and significantly fewer nuclei were found in diabetic retina. Moreover, the diabetic retina also presented increased ROS generation and more TUNEL-positive cells. Probucol treatment prevented diabetes-induced lesions. In addition, the treatment also upregulated Nrf2 expression in diabetic retina. It was suggested that probucol attenuated diabetes-induced retinal neuronal degeneration via upregulating the Nrf2 signaling pathway possibly. Probucol may be repurposed for DR management. [ABSTRACT FROM AUTHOR]

Purpose: Toll-like receptor 5 (TLR5) is a pattern recognition receptor and plays key roles in inflammatory responses against pathogen infection. Recent evidence suggests that TLR5 is expressed in a wide variety of tumors and exhibits either pro-tumor or anti-tumor activities. In this study, we explored expression of TLR5 in the context of non-small-cell lung cancer (NSCLC) and evaluated the effects of TLR5 signaling in NSCLC cells. Methods: The lung carcinoma samples were collected from 113 patients diagnosed as NSCLC at Tumor Hospital of Xiangya School of Medicine from January 2005 to December 2008. Immunohistochemistry was performed for TLR5 and the protein expression score was quantified using an established scoring system. Kaplan-Meier survival curves were generated for disease-free survival (DFS) and overall survival (OS) in all patients. TLR5 expression levels were correlated with DFS and OS using univariate and multivariate Cox regression analysis. Expression and subcellular localization of TLR5 were analyzed in NSCLC cell lines including SPC-A1, A549, H1975, and H1299 cells. Activation of TLR5 signaling pathway by flagellin was characterized by western blotting. Effects of flagellin on NSCLC cell proliferation, anchorage-independent growth, migration, and invasion were analyzed by BrdU incorporation assay, soft agar colony formation assay, wound-healing migration assay, and transwell invasion assay, respectively. Results: High expression of TLR5 was significantly associated with better prognosis in patients with NSCLC. We further demonstrated that activation of TLR5 by flagellin in NSCLC cells inhibited cell proliferation, migration, and invasion in vitro. Conclusion: TLR5 may serve as a potential therapeutic target in NSCLC patients. [ABSTRACT FROM AUTHOR]