The impact of urinary albumin-creatinine ratio and glomerular filtration rate on long-term mortality in patients with heart failure: The National Health and Nutrition Examination Survey 1999-2018.

BACKGROUND AND AIMS: The urinary albumin‒creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR) are important markers of renal dysfunction, but few studies have simultaneously examined their impact on long-term mortality in patients with heart failure (HF). METHODS AND RESULTS: This study included patients with HF from the National Health and Nutrition Survey from 1999 to 2018. The fully adjusted Cox proportional risk model was adopted, and propensity score matching (PSM) was also used for risk adjustment. Among 988 patients, a median follow-up of 7.75 years was recorded. A higher UACR corresponded to a higher risk of cardiovascular death (P < 0.001 for trend). No statistically significant difference was found in the trend of eGFR risk stratification on the risk of cardiovascular death (P = 0.09 for trend). After PSM, the results showed that when grouped by UACR, the high-risk group had a higher risk of cardiovascular death regardless of a cutoff value of 30 or 300 mg/g (all P < 0.05). When grouped by eGFR, regardless of a cutoff value of 45 or 30 mL/min/1.73 m2, compared to the low-risk group, the high-risk group did not have a statistically significant increase in cardiovascular death (P = 0.086 and P = 0.093, respectively). The subgroup analysis of the main outcome showed an interaction between the UACR and eGFR (P = 0.044). CONCLUSIONS: Both the UACR and eGFR are markers for predicting the progression of HF, but the UACR may be a more important indicator than the eGFR, and they synergistically and complementarily reflect the long-term cardiovascular risk of HF patients.

Exosomes from ectopic endometrial stromal cells promote M2 macrophage polarization by delivering miR-146a-5p.

BACKGROUND: Ectopic endometrial stromal cells (ESCs) and M2 macrophages co-exist in the lesions of endometriosis and participate in the occurrence and progression of endometriosis. However, the interaction between ectopic ESCs and M2-type macrophage polarization is poorly understood. This study aims to investigate the effect of exosomes released from ectopic ESCs on M2 macrophage polarization and the potential mechanism. METHODS: Human THP-1 monocytic cells induced macrophage differentiation (M0) and M2 polarization. Ectopic ESCs and their exosomes were used to stimulate M2 macrophages. M2 macrophage polarization was examined by detecting CD163 and ARG1 expression. Exosomal microRNAs were analyzed by small-RNA sequencing. RESULTS: Our in vitro results suggest that exosomes of ectopic ESCs promoted M2 macrophage polarization. Meanwhile, The miR-146a-5p level was highly increased in ectopic ESCs and their exosomes and promoted the role of exosomes in M2 macrophage polarization. As a target, TRAF6 overexpression inhibits the function of miR-146a-5p mimic on M2 macrophage polarization. In the rat model, exosomes from ectopic ESCs contribute to the development of endometriosis. CONCLUSIONS: It was suggested that exosomes derived from ectopic ESCs promote the M2 macrophage polarization by delivering miR-146a-5p targeting TRAF6 in the pathological process of endometriosis.

Lipid Profiling Reveals Lipidomic Signatures of Weight Loss Interventions.

Obesity is an epidemic all around the world. Weight loss interventions that are effective differ from each other with regard to various lipidomic responses. Here, we aimed to find lipidomic biomarkers that are related to beneficial changes in weight loss. We adopted an untargeted liquid chromatography with tandem mass spectrometry (LC-MS/MS) method to measure 953 lipid species for Exercise (exercise intervention cohort, N = 25), 1388 lipid species for LSG (laparoscopic sleeve gastrectomy cohort, N = 36), and 886 lipid species for Cushing (surgical removal of the ACTH-secreting pituitary adenomas cohort, N = 25). Overall, the total diacylglycerol (DG), triacylglycerol (TG), phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylserine (PS), and sphingomyelin (SM) levels were associated with changes in BMI, glycated hemoglobin (HbA1c), triglyceride, and total cholesterol according to weight loss interventions. We found that 73 lipid species changed among the three weight loss interventions. We screened 13 lipid species with better predictive accuracy in diagnosing weight loss situations in either Exercise, LSG, or Cushing cohorts (AUROC > 0.7). More importantly, we identified three phosphatidylcholine (PC) lipid species, PC (14:0_18:3), PC (31:1), and PC (32:2) that were significantly associated with weight change in three studies. Our results highlight potential lipidomic biomarkers that, in the future, could be used in personalized approaches involving weight loss interventions.

Exercise-induced microbial changes in preventing type 2 diabetes.

The metabolic benefits associated with long-term physical activity are well appreciated and growing evidence suggests that it involves the gut microbiota. Here we re-evaluated the link between exercise-induced microbial changes and those associated with prediabetes and diabetes. We found that the relative abundances of substantial amounts of diabetes-associated metagenomic species associated negatively with physical fitness in a Chinese athlete students cohort. We additionally showed that those microbial changes correlated more with handgrip strength, a simple but valuable biomarker suggestive of the diabetes states, than maximum oxygen intake, one of the key surrogates for endurance training. Moreover, the causal relationships among exercise, risks for diabetes, and gut microbiota were explored based on mediation analysis. We propose that the protective roles of exercise against type 2 diabetes are mediated, at least partly, by the gut microbiota.

Hypoxia as a Double-Edged Sword to Combat Obesity and Comorbidities.

The global epidemic of obesity is tightly associated with numerous comorbidities, such as type II diabetes, cardiovascular diseases and the metabolic syndrome. Among the key features of obesity, some studies have suggested the abnormal expansion of adipose-tissue-induced local endogenous hypoxic, while other studies indicated endogenous hyperoxia as the opposite trend. Endogenous hypoxic aggravates dysfunction in adipose tissue and stimulates secretion of inflammatory molecules, which contribute to obesity. In contrast, hypoxic exposure combined with training effectively generate exogenous hypoxic to reduce body weight and downregulate metabolic risks. The (patho)physiological effects in adipose tissue are distinct from those of endogenous hypoxic. We critically assess the latest advances on the molecular mediators of endogenous hypoxic that regulate the dysfunction in adipose tissue. Subsequently we propose potential therapeutic targets in adipose tissues and the small molecules that may reverse the detrimental effect of local endogenous hypoxic. More importantly, we discuss alterations of metabolic pathways in adipose tissue and the metabolic benefits brought by hypoxic exercise. In terms of therapeutic intervention, numerous approaches have been developed to treat obesity, nevertheless durability and safety remain the major concern. Thus, a combination of the therapies that suppress endogenous hypoxic with exercise plans that augment exogenous hypoxic may accelerate the development of more effective and durable medications to treat obesity and comorbidities.

Plasma Metabolomics Reveals ß-Glucan Improves Muscle Strength and Exercise Capacity in Athletes.

The present study aimed to assess the changes in muscle strength and plasma metabolites in athletes with ß-glucan supplementation. A total of 29 athletes who met the inclusion criteria were recruited for this study (ChiCTR2200058091) and were randomly divided into a placebo group (n = 14) and ß-glucan group (n = 15). During the trial, the experimental group received ß-glucan supplementation (2 g/d ß-glucan) for 4 weeks and the control group received an equal dose of placebo supplementation (0 g/d ß-glucan), with both groups maintaining their regular diet and exercise habits during the trial. The athletes' exercise performance, muscle strength, and plasma metabolome changes were analyzed after 4 weeks of ß-glucan supplementation. The results showed a significant increase in mean grip strength (kg), right hand grip strength (kg), left triceps strength (kg), and upper limb muscle mass (kg) in the experimental group after the 4-week intervention compared to the preintervention period (p < 0.05). A comparison of the difference between the two groups after the intervention showed that there were significant differences between the control group and the experimental group in mean grip strength (kg) and right-hand grip strength (kg) (p < 0.05). Athletes in the experimental group showed significant improvements in 1 min double rocking jump (pcs), VO2max (ml/kg-min) (p < 0.05). The ß-glucan intake increased the creatine-related pathway metabolites in plasma. Overall, these results suggest that 4 weeks of ß-glucan supplementation can improve muscle strength in athletes, with the potential to increase aerobic endurance and enhance immune function, possibly by affecting creatine-related pathways.

Trends and Outcomes of Hospitalized Influenza Patients With End-Stage Kidney Disease: Insights From the National Inpatient Sample 2010-2019.

Introduction Influenza causes significant morbidity and mortality annually in the United States (US) and people with chronic medical conditions are thought to be at higher risk for severe disease and death. Infection is a leading cause of death for patients with end-stage kidney disease (ESKD). We used a national-level inpatient database to study the trend of influenza hospitalizations and in-hospital mortality for patients without and with ESKD. Methods The National Inpatient Sample (NIS) 2010-2019 was used. A primary diagnosis of influenza was identified using ICD-9-CM (487.X, 488.X) and ICD-10-CM codes (J09.X, J10.X, J11.X). ESKD was identified using a validated algorithm identifying patients with a diagnosis of ESKD or procedure code for dialysis and excluding patients with a diagnosis of acute kidney injury. Other diagnoses and procedures were identified using validated algorithms based on ICD-9-CM, ICD-10-CM, and ICD-10-PCS codes. Discharge-level weights were used to estimate the total number of admissions in the NIS universe. Weighted multivariable logistic regression was performed to study the association between ESKD and in-hospital death. Results 131,942 admissions with a primary diagnosis of influenza with 4,647 admissions for ESKD patients among them were included in our analysis. Admissions varied by influenza season and ESKD patients accounted for 2.91% to 3.65% of all influenza admissions each season. 2,081 influenza patients (1.58%) died in the hospital and 115 patients with influenza and ESKD (2.47%) died in the hospital. Age-adjusted in-hospital mortality varied from season to season but was consistently higher in ESKD patients (2.25% vs 1.38%). ESKD was a risk factor for in-hospital death (OR 1.26, 95% CI 1.15-1.38) after adjusting for age, gender, primary payer, heart failure, chronic lung disease, obesity, drug abuse, immunocompromised status, bacterial pneumonia, the Charlson Comorbidity Index, and the influenza season. Conclusion ESKD patients accounted for a significant proportion of influenza hospitalizations in the US from 2010-11 to the 2018-19 influenza season. Among people hospitalized primarily for influenza, age-adjusted in-hospital mortality varied from season to season and was consistently higher in ESKD patients. For people hospitalized primarily for influenza, ESKD was an independent risk factor for in-hospital death.

The Efficacy of Tai Chi and Stretching Exercises Based on a Smartphone Application for Patients With Parkinson's Disease: A Protocol for a Randomized Controlled Trial.

Introduction: Parkinson's disease (PD) is a common neurodegenerative disease that seriously impairs patients' quality of life, and increases the burden of patients and caregivers. Both drugs and exercise can alleviate its motor and non-motor symptoms, improving the quality of life for PD patients. Telehealth, an increasingly popular tool, makes rehabilitation accessible at home, overcoming the inconvenience of traffic and scheduling. Care-PD is a phone application designed for rehabilitation training, which provides Tai Chi and stretching exercises through tutorial videos as well as an online evaluation system. In this protocol, we will explore the efficacy of Tai Chi and stretching exercises as a PD rehabilitation therapy based on the smartphone application Care-PD. Methods and Analysis: A double-blind, parallel randomized controlled trial will be conducted in this study. The recruitment, intervention, and evaluation processes will be implemented through the Care-PD application. Persons with PD will fill out questionnaires on Activities of Daily Living (ADL), upload the latest case report, and sign the informed consent form in the application. Afterward, doctors and researchers will screen and enroll 180 participants who will be randomly (1:1:1) assigned to Tai Chi group, stretching exercises group, or control group. The subjects will participate in a 1-h exercise session three times per week for 12 weeks, ending with another 4 weeks of follow-up study. Each exercise session includes 10 min of warm-up, 45 min of exercise, and 5 min of cool-down. The primary outcomes are Motor Aspects of Experiences of Daily Living and the 39-item Parkinson's disease Questionnaire. The secondary outcomes include the 9-item Wearing-Off Questionnaire, the Freezing of Gait Questionnaire, the Caregiver Strain Index, Non-motor Experiences of Daily Living, ADL, and Morse Fall Scale. All assessments will be performed at baseline, week 12 and 16. Discussion: Care-PD integrates subject recruitment, intervention, and evaluation, providing a new perspective on clinical rehabilitation for persons with PD. This study will evaluate the efficacy of Tai Chi and stretching exercises on patients' quality of life and disease progression based on a smartphone application. We aim to provide a new rehabilitation training platform for persons with PD. Ethics and Dissemination: This study was approved by the Scientific Research Ethics Committee (102772020RT132) of Shanghai University of Sport. Data collection begins after the approval of the ethics committee. The participants must sign an informed consent form before enrollment. The results will be published in relevant journals, seminars, and be disseminated among rehabilitation practitioners and patients with PD. Clinical Trial Registration: Chinese Clinical Trial Registry, identifier [ChiCTR2100042096]. Registered on January 13, 2021.

Gastrointestinal bleeding is associated with higher in-hospital mortality, longer length of stay and higher cost in patients with in-hospital cardiac arrest.

BACKGROUND: In-hospital cardiac arrest (IHCA) carries a high mortality and significant morbidity in survivors. Gastrointestinal bleeding (GIB) can complicate cardiac arrests. We aim to study the association between GIB and the in-hospital outcomes of patients with IHCA. METHODS AND RESULTS: The National Inpatient Sample 2016-2018 databases were used. IHCA were identified using ICD-10-PCS code for cardiopulmonary resuscitation. Other diagnoses including GIB were identified using ICD-10-CM codes. Multivariate logistic regression was used to study the effect of GIB on in-hospital mortality. Gamma regression with log link was used to determine the effect of GIB on length of stay and cost of admission. In patients with IHCA, GIB as a secondary diagnosis is associated with an increased in hospital mortality (unadjusted 74.2% vs 68.3%, adjusted OR 1.17, 95% confidence interval [CI] 1.09-1.25, p < 0.001), longer length of stay (unadjusted median 16 vs 10 days, IQR 9-27 vs 5-17 days, exponentiated coefficient 1.45, 95% CI 1.36-1.54, p < 0.001 for survivors; unadjusted median 4 vs 3 days, IQR 1-10 vs 1-7 days, exponentiated coefficient 1.27, 95% CI 1.22-1.34, p < 0.001 for patients who died in hospital), and higher cost for hospital stay (unadjusted median $226065 vs $151459, IQR $117551-434003 vs $76197-287846, exponentiated coefficient 1.40, 95% CI 1.32-1.49, p < 0.001 for survivors; unadjusted median $87996 vs $77056, IQR $42566-186677 vs $34066-149009, exponentiated coefficient 1.26, 95% CI 1.20-1.32, p < 0.001 for patients who died in hospital) adjusted for baseline characteristics and other comorbidities. CONCLUSIONS: In patients with IHCA, GIB as a secondary diagnosis is associated with a higher in-hospital mortality, longer length of stay and higher cost for the admission.

Tea Consumption and the Risk of Endometrial Cancer: An Updated Meta-Analysis.

Although the relationship between tea consumption and the risk of endometrial cancer has been previously analyzed in certain studies, the resulting information is still conflicting, and a previous meta-analysis yielded inconsistent results. Therefore, here, we aimed to perform an updated meta-analysis of studies on this subject in order to elucidate this relationship.We searched the literature on the PubMed, Web of Science, Scopus, and Chinese National Knowledge Infrastructure databases for studies that were published prior to September 25, 2019, and all the relevant references were examined. Ultimately, we included eight studies, and seven of them were on black tea. We used the overall relative risk values (RR) and 95% confidence intervals (CI) to evaluate the risk. The synthetic RR of the eight eligible studies demonstrated that tea consumption was not relevant to the incidence rate of endometrial cancer (RR 1.06, 95% CI 0.96, 1.18). No publication bias was found. We detected significant heterogeneity among the studies (Q = 15.84, p = 0.027, I2 = 55.8%). In conclusion, the results of this meta-analysis indicate that tea consumption is not relevant to the incidence of endometrial cancer. Further research and cohort studies should be conducted to validate our result.

Identification of key genes and pathways in endometriosis by integrated expression profiles analysis.

The purpose of this study was to integrate the existing expression profile data on endometriosis (EM)-related tissues in order to identify the differentially expressed genes. In this study, three series of raw expression data were downloaded from GEO database. Differentially expressed genes (DEGs) in three tissue types were screened. GO, KEGG pathway enrichment analysis, core differential genes (CDGs) protein-protein interaction (PPI) network and weighted gene co-expression network analysis (WGCNA) were performed, finally, the dysregulation of Hippo pathway in ectopic endometrium (EC) was detected by Western blotting. A total of 1,811 DEGs between eutopic (EU) and normal endometrium (NE), 5,947 DEGs between EC and EU, and 3,192 DEGs between EC and NE datasets were identified. After screening, 394 CDGs were obtained, and 5 hub genes identified in the PPI network. CDGs enrichment and WGCNA network analysis revealed cell proliferation, differentiation, migration and other biological processes, Hippo and Wnt signaling pathways, and a variety of tumor-related pathways. Western blotting results showed that YAP/TAZ was upregulated, and MOB1, pMOB1, SAV1, LATS1 and LATS2 were downregulated in EC. Moreover, CDGs, especially the hub genes, are potential biomarkers and therapeutic targets. Finally, the Hippo pathway might play a key role in the development of endometriosis.

Epidermal growth factor promotes stromal cells migration and invasion via up-regulation of hyaluronate synthase 2 and hyaluronan in endometriosis.

OBJECTIVE: To investigate the role(s) of hyaluronan synthase 2 (HAS2) and hyaluronan in disease progression of endometriosis and epidermal growth factor (EGF)-induced motility changes of endometriotic cells. DESIGN: A case-control experimental study and in vitro primary cell culture study. SETTING: University hospital-affiliated research centers. PATIENTS: A total of 21 women with stage I/II endometriosis, 33 women with stage III/IV endometriosis with endometrioma, and 32 women without endometriosis were included in our study. INTERVENTIONS: Serum, eutopic endometrial tissues, and/or ectopic endometriotic tissues were collected. Primary eutopic endometrial stromal cells (EuESCs) and ectopic ovarian endometriotic stromal cells (OvESCs) were isolated and cultured from women with ovarian endometrioma, and then treated with or without EGF. MAIN OUTCOME MEASURES: The concentrations of EGF and hyaluronan in serum were analyzed by enzyme-linked immunosorbent assay. The expressions and localizations of EGF receptor (EGFR), phosphorylated-(p)EGFR, HAS2, and hyaluronan receptor CD44 in tissues were examined by immunohistochemistry. The mRNA and protein levels of HAS2 in EuESCs and OvESCs were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot, respectively, and the concentrations of hyaluronan in conditioned medium were examined by enzyme-linked immunosorbent assay (ELISA). Cell motility was evaluated by transwell migration/invasion assays. RESULTS: Serum EGF and hyaluronan concentrations were higher in women with stage III/IV endometriosis than in women with stage I/II or without endometriosis. EGFR, pEGFR, HAS2, and CD44 were immunolocalized in eutopic endometrium and ectopic endometriotic lesions, and the expressions of pEGFR and HAS2 were elevated in ectopic endometriotic lesions compared to eutopic endometrium. Treatment with EGF upregulated HAS2 and hyaluronan expression as well as cell migration and invasion in both EuESCs and OvESCs, and pharmaceutical blocking of EGFR abolished these effects. In addition, knockdown of HAS2 by small interfering RNA attenuated both basal and EGF-induced hyaluronan expression and cell motility changes. Notably, ERK1/2 and AKT signaling pathways were shown to be downstream of EGF in regulating HAS2 and hyaluronan expression as well as cell migration and invasion. CONCLUSION: EGF increased the expression of endometriosis-associated hyaluronan and its synthase HAS2, both of which mediated EGF-induced stromal cell migration and invasion in women with endometriosis.

Autocrine Production of Interleukin-34 Promotes the Development of Endometriosis through CSF1R/JAK3/STAT6 signaling.

Interleukin (IL)-34 plays a critical role in cell proliferation, differentiation, apoptosis, angiogenesis, inflammation and immunoregulation. Numerous diseases can be attributed to the dysregulation of IL-34 signaling. This study was performed to investigate the function of IL-34 in the pathogenesis of endometriosis. Firstly, by enzyme linked immunoabsorbent assay, we found that IL-34, VEGF, MMP-2 and MMP-9 were increased in the sera of patients with endometriosis. Secondly, exposure to IL-34 promoted the proliferation, migration and invasion of eutopic endometrial stromal cells (ESCs). Additionally, stimulation with IL-34 up-regulated colony-stimulating factor 1 receptor (CSF1R), p-JAK3, p-STAT6, VEGF, MMP-2 and MMP-9 in these eutopic ESCs. Treatment with AS1517499, an inhibitor of STAT6, remarkably abrogated the alterations induced by IL-34. A Chromatin immunoprecipitation (ChIP) assay demonstrated binding of STAT6 to the IL-34 promoter, further implicating STAT6 in IL-34 signaling. Notably, reverse results were obtained in ectopic ESCs with the application of an IL-34 neutralizing antibody. In vivo, AS1517499 suppressed the maintenance of endometriosis lesions in rats. In summary, autocrine production of IL-34, mediated by STAT6, promoted the development of endometriosis in vitro and in vivo through the CSF1R/JAK3/STAT6 pathway. Our research reveals the function of IL-34 in endometriosis, which may provide insight into novel therapeutic strategies for endometriosis.

Analysis of long non-coding RNA expression profiles using RNA sequencing in ovarian endometriosis.

Endometriosis is a common gynecological condition with unclear pathogenesis. Although a dysregulated lncRNA expression profile has been speculated, very few studies have addressed this hypothesis. We determined the differential lncRNA and mRNA expression patterns between endometriosis and control tissues, and between eutopic and normal endometrium in the proliferative phase, using RNA sequencing. The potential targets of lncRNA were predicted on the basis of cis and trans action, and lncRNAs were functionally annotated in relation to their co-expressed mRNAs. Dysregulated lncRNAs and mRNAs were screened relative to the biological features of endometriosis, and the five filtered lncRNAs were validated using qRT-PCR. A total of 9924 novel lncRNA transcripts were identified, and 86 lncRNAs and 1228 mRNAs were differentially expressed between the endometriosis and control groups. GO and KEGG pathway analysis showed that the differentially expressed lncRNAs were enriched in the biological processes and signaling pathways involved in endometriosis. A coding-noncoding gene (CNC) co-expression network was constructed using the dysregulated lncRNAs and their co-expressed mRNAs to simulate the complex intergenic interactions. This study is the first to use sequencing technology to elucidate the differentially lncRNA expression profiles of eutopic and normal endometrium in the proliferative phase of endometriosis. The dysregulated lncRNAs can potentially be novel diagnostic biomarkers and therapeutic targets of endometriosis.

Upregulation of S100A6 in patients with endometriosis and its role in ectopic endometrial stromal cells.

S100 calcium-binding protein A6 (S100A6) is up-regulated in many malignancies and overexpression of S100A6 has been identified associated with proliferation, migration and invasion phenotype in several cancer cells. In the present study, we explored whether S100A6 plays a role in the development of endometriosis. Significantly higher levels of mRNA and protein expression of S100A6 were observed in ectopic endometrial tissues compared to eutopic and normal endometrial tissues. Silencing of S100A6 in ectopic endometrial stromal cells (ESCs) significantly inhibited cell viability, migration and invasion. Moreover, knockdown of S100A6 suppressed p38/MAPK activity in ectopic ESCs, which can be partially attenuated by CacyBP/SIP phosphorylation inhibitor. In conclusion, our results suggest that the abnormal expression of S100A6 may contribute to the pathogenesis of endometriosis and the S100A6/CacyBP/p38 signaling may provide as a promising treatment target.

Silencing of SRA1 Regulates ER Expression and Attenuates the Growth of Stromal Cells in Ovarian Endometriosis.

Estradiol and its nuclear receptors, estrogen receptor (ER) α and ER-ß, have important functions in endometriosis, and the transcriptional activity of these receptors is modulated by coactivators and corepressors. The steroid receptor RNA activator 1 (SRA1) produces SRA long noncoding RNA (lncRNA) and SRA protein (SRAP), which regulate ER expression at the RNA and protein levels in some hormone-dependent tumors via an alternative splicing event. However, only a few are reported on their expressions in endometriosis. Here, we observed that low expression levels of SRA lncRNA and ER-α but relatively high expression levels of SRAP and ER-ß were detected in ovarian endometriotic tissues versus normal endometrial tissues. Steroid receptor RNA activator 1-small interfering RNA treatment significantly increased ER-α levels but reduced ER-ß levels in endometriotic stromal cells (ESCs). Furthermore, the treatment can also attenuate the proliferation and promote early apoptosis in these cells. Our results indicate that the regulation of ER via SRA in ovarian endometriosis may play a significant role in the growth of ESCs.

[Sodium cromoglycate attenuates experimental endometriosis in rats by regulating mast cells].

OBJECTIVE: To investigate the effect of sodium cromoglycate on experimental endometriosis in rats. METHODS: Endometriosis model was established in 36 unpregnant female SD rats by transplanting autologous fragments of endometrium to the inner surface of the abdominal wall. The endometriotic lesions were measured by a second laparotomy 2 weeks after surgery. Then the rats were randomly divided into four groups (n=8 in each group) to receive intraperitoneal injection of different doses of sodium cromoglycate for 2 weeks: high-dose group (20 mg·kg⁻¹·d⁻¹); low-dose group (10 mg·kg⁻¹·d⁻¹); the negative control group and the blank control group. The animals were sacrificed and the size of the lesions were measured. The endometriosis model of SD rats was identified by HE staining and immunohistochemical staining of keratin and vimentin. The total number of mast cells and their degranulation were measured by Toluidine blue staining; the concentrations of TNF-α in serum were measured by enzyme linked immunosorbent assay; the concentrations of estradiol in serum were measured by enzyme immunoassay; the expression of tryptase and nerve growth factor (NGF) were measured by immunohistochemical staining. RESULTS: The number of activated mast cells (MC) by Toluidine blue staining in high-dose group was significantly lower than that in negative control group (P<0.05), and its ratio of degranulation/total number of MC was significantly lower than that in negative control group or blank control group (P<0.05). The serum TNF-α levels and tryptase expression in tissues in high-dose group were significantly lower than those in negative control group or blank control group (P<0.05). However, no significant difference in the size of endometriotic lesions and expression of NGF was found among groups (P>0.05). CONCLUSION: Sodium cromoglycate can stabilize mast cells from degranulation, which may relieve the clinical symptoms of endometriosis by reducing TNF-α and tryptase levels.