Objective To explore the effect of evening primrose oil(EPO)on aortic endothelial damage in rats with polycystic ovary syndrome(PCOS),using network pharmacology and in vivo experiments.Methods The potential targets of EPO for improving aortic endothelial injury in PCOS rats were predicted by network pharmacology,and the selected core targets and renin-angiotensin signaling(RAS)pathway were verified by experiments.Fifty-eight female SD rats were divided randomly into a blank group(n=10)and a modeling group(n=48).Rats in the blank group were fed a normal diet and rats in the modeling group received a high-fat diet for 8 weeks.The PCOS model was prepared at week 6 by administration of letrozole(1 mg/(kg·d))for 21 days.Blood was taken from the tail vein after modeling and serum was collected to detect hormone levels.The model rats were then divided randomly into four groups and treated with the corresponding drugs for 6 weeks.Blood,blood vessels,and ovaries were then collected.Tissue morphology was examined by hematoxylin and eosin staining and serum levels of luteinizing hormone(LH),testosterone(T),follicle-stimulating hormone(FSH),endothelin(ET-1),and tumor necrosis factor(TNF-α)were detected by enzyme-linked immunosorbent assay(ELISA).Serum levels of nitric oxide(NO)were determined by spectrophotometry.Protein expression levels of core targets and RAS pathway-related factors were assessed by western blotting and immunohistochemistry.Results Twenty-five intersection targets of EPO and PCOS were identified by network pharmacological analysis.Kyoto encyclopedia of genes and genomes analysis showed that EPO improved vascular injury in PCOS rats via multiple pathways,including RAS.Serum levels of ET-1,FSH,LH,and T measured by ELISA were significantly decreased after EPO treatment,compared with the model group(P＜0.01).EPO significantly decreased the expression levels of Ang Ⅰ,VEGF-B,AT2R,ET-1,and TNF-α proteins in the aorta(P＜0.01)and significantly increased expression levels of Ang Ⅱ,CD31,and endothelial NO synthase proteins(P＜0.01).Conclusions EPO may ameliorate vascular endothelial injury in PCOS model rats by inhibiting the RAS signaling pathway and by overactivation of the ACE/Ang Ⅱ/AT1 axis.

To investigate the protective effect of Lycium barbarum glycopeptide(LbGp)on testicu-lar injury induced by D-galactose(D-gal)in aging rats,male SD rats were randomly divided into 6 groups:the blank control group(Control),aging model group(Model),positive control group(β-nicotinamide mononucleotide,NMN),low dose LbGp group(LLbGp),medium dose LbGp group(MLbGp)and high dose LbGp group(HLbGp).The testicular mass of rats was counted,the morphological changes of testicular tissue were observed by hematoxylin-eosin(HE)staining,the testicular senescence was detected by β-galactosidase(SA-β-gal)staining,and the levels of testos-terone(T),luteinizing hormone(LH)and follicle stimulating hormone(FSH)in serum were de-tected.The levels of oxidative factors such as glutathione peroxidase(GSH-Px),superoxide dis-mutase(SOD),malondialdehyde(MDA),catalase(CAT)and inflammatory factors such as tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6)in rat tissues were measured.TUNEL staining was used to detect the apoptosis of testicular cells,epididymal sperm quality,and the expression of Keap1,Nrf2 and Nqo1 mRNA were analyzed.The results showed that compared with the Model group,the testicular coefficient of Lycium barbarum glycopeptide rats in MLbGp and HLbGp groups increased(P＜0.01),the level of T in serum and sperm quality increased(P＜0.05),the structural degeneration and aging of testicular tissue decreased(P＜0.01),the level of antioxidant factors increased,and the levels of inflammatory factors and apopto-sis decreased(P＜0.05).The expression of Keap1 decreased significantly(P＜0.01),while the ex-pression of Nrf2 and Nqo1 mRNA increased(P＜0.05).The above results indicate that Lycium barbarum glycopeptide can improve D-gal-induced testicular senescence,attenuate oxidative stress,reduce inflammatory response,decrease apoptosis,and exert a protective effect on testicular injury in rats due to senescence through the Keap1-Nrf2 signaling pathway.

To investigate the protective effect of Lycium barbarum glycopeptide(LbGp)on testicu-lar injury induced by D-galactose(D-gal)in aging rats,male SD rats were randomly divided into 6 groups:the blank control group(Control),aging model group(Model),positive control group(β-nicotinamide mononucleotide,NMN),low dose LbGp group(LLbGp),medium dose LbGp group(MLbGp)and high dose LbGp group(HLbGp).The testicular mass of rats was counted,the morphological changes of testicular tissue were observed by hematoxylin-eosin(HE)staining,the testicular senescence was detected by β-galactosidase(SA-β-gal)staining,and the levels of testos-terone(T),luteinizing hormone(LH)and follicle stimulating hormone(FSH)in serum were de-tected.The levels of oxidative factors such as glutathione peroxidase(GSH-Px),superoxide dis-mutase(SOD),malondialdehyde(MDA),catalase(CAT)and inflammatory factors such as tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6)in rat tissues were measured.TUNEL staining was used to detect the apoptosis of testicular cells,epididymal sperm quality,and the expression of Keap1,Nrf2 and Nqo1 mRNA were analyzed.The results showed that compared with the Model group,the testicular coefficient of Lycium barbarum glycopeptide rats in MLbGp and HLbGp groups increased(P＜0.01),the level of T in serum and sperm quality increased(P＜0.05),the structural degeneration and aging of testicular tissue decreased(P＜0.01),the level of antioxidant factors increased,and the levels of inflammatory factors and apopto-sis decreased(P＜0.05).The expression of Keap1 decreased significantly(P＜0.01),while the ex-pression of Nrf2 and Nqo1 mRNA increased(P＜0.05).The above results indicate that Lycium barbarum glycopeptide can improve D-gal-induced testicular senescence,attenuate oxidative stress,reduce inflammatory response,decrease apoptosis,and exert a protective effect on testicular injury in rats due to senescence through the Keap1-Nrf2 signaling pathway.

Objective To explore the effect of evening primrose oil(EPO)on aortic endothelial damage in rats with polycystic ovary syndrome(PCOS),using network pharmacology and in vivo experiments.Methods The potential targets of EPO for improving aortic endothelial injury in PCOS rats were predicted by network pharmacology,and the selected core targets and renin-angiotensin signaling(RAS)pathway were verified by experiments.Fifty-eight female SD rats were divided randomly into a blank group(n=10)and a modeling group(n=48).Rats in the blank group were fed a normal diet and rats in the modeling group received a high-fat diet for 8 weeks.The PCOS model was prepared at week 6 by administration of letrozole(1 mg/(kg·d))for 21 days.Blood was taken from the tail vein after modeling and serum was collected to detect hormone levels.The model rats were then divided randomly into four groups and treated with the corresponding drugs for 6 weeks.Blood,blood vessels,and ovaries were then collected.Tissue morphology was examined by hematoxylin and eosin staining and serum levels of luteinizing hormone(LH),testosterone(T),follicle-stimulating hormone(FSH),endothelin(ET-1),and tumor necrosis factor(TNF-α)were detected by enzyme-linked immunosorbent assay(ELISA).Serum levels of nitric oxide(NO)were determined by spectrophotometry.Protein expression levels of core targets and RAS pathway-related factors were assessed by western blotting and immunohistochemistry.Results Twenty-five intersection targets of EPO and PCOS were identified by network pharmacological analysis.Kyoto encyclopedia of genes and genomes analysis showed that EPO improved vascular injury in PCOS rats via multiple pathways,including RAS.Serum levels of ET-1,FSH,LH,and T measured by ELISA were significantly decreased after EPO treatment,compared with the model group(P＜0.01).EPO significantly decreased the expression levels of Ang Ⅰ,VEGF-B,AT2R,ET-1,and TNF-α proteins in the aorta(P＜0.01)and significantly increased expression levels of Ang Ⅱ,CD31,and endothelial NO synthase proteins(P＜0.01).Conclusions EPO may ameliorate vascular endothelial injury in PCOS model rats by inhibiting the RAS signaling pathway and by overactivation of the ACE/Ang Ⅱ/AT1 axis.

Objective: To investigate the health literacy and its influencing factors among residents in areas out of poverty in Kunming City, so as to provide insights into formulating health education strategies. Methods: A total of 1 916 permanent residents at ages of 15 to 69 years were sampled in three areas out of poverty in Kunming City using the multi-stage stratified random sampling method and probability proportionate to size sampling method from August to October, 2020. Health literacy was investigated using the Questionnaire on the Health Literacy among Chinese Residents, the level of health literacy was analyzed and weighted by the population of the China's Seventh National Population Census. Factors affecting health literacy among residents in areas out of poverty were identified using a multivariable logistic regression model. Results: A total of 1 916 questionnaires were allocated, and 1 908 valid questionnaires were recovered, with an effective recovery rate of 99.58%. The respondents included 997 men (52.25%) and 911 women (47.75%), and had a mean age of (45.58±14.28) years. The level of health literacy was 21.38%. Multivariable logistic regression analysis identified age (15 to 24 years, OR=5.087, 95%CI: 1.573-16.450; 25 to 34 years, OR=6.016, 95%CI: 1.991-18.183; 35 to 44 years, OR=7.526, 95%CI: 2.541-22.289; 45 to 54 years, OR=4.800, 95%CI: 1.640-14.050), educational level (junior high school, OR=5.333, 95%CI: 3.100-9.175; high school/vocational high school/technical secondary school, OR=19.895, 95%CI: 10.418-37.966; college or above, OR=27.580, 95%CI: 12.349-61.597) as factors affecting health literacy among residents in areas out of poverty in Kunming City. Conclusion The level of health literacy is 21.38% among residents in areas out of poverty in Kunming City, and age and educational level are associated factors.

AIM: To investigate the role of ribonucleotide reductase M2 (RRM2) in 5-fluorouracil (5-FU) resistance of HCC cells and to develop potential strategies to enhance the sensitivity of HCC cells to 5-FU. METHODS: The expression of RRM2 was examined by Western blot in BEL/5-FU cells and BEL7402 cells. The expression of RRM2 was down-regulated through RNA interference (RNAi) technology and the activity of RRM2 was inhibited by the RRM2 inhibitor 3-AP. The cell proliferation ability was detected by CCK-8 assay and colony formation assay, and the apoptosis was analyzed by Confocal high-content system. RESULTS: The expression level of RRM2 was increased by 2.5-fold in BEL/5-FU cells compared with BEL7402 cells. Compared with control siRNA, the half maximum inhibitory concentration IC

OBJECTIVE: The present study is to evaluate the biological functions of long non-coding RNA (lncRNA), X-inactive specific transcript, X-inactive specific transcript (XIST) in human epithelial ovarian cancer (EOC). METHODS: XIST was upregulated in EOC cell lines, CAOV3 and OVCAR3 cells by lentiviral transduction. The effects of XIST overexpression on cancer cell proliferation, invasion, chemosensitivity and in vivo tumor growth were investigated, respectively. Possible sponging interaction between XIST and human microRNA hsa-miR-214-3p was further evaluated. Furthermore, hsa-miR-214-3p was overexpressed in XIST-upregulated CAOV3 and OVCAR3 cells to evaluate its effect on XIST-mediated EOC regulation. RESULTS: Lentivirus-mediated XIST upregulation had significant anticancer effects in CAOV3 and OVCAR3 cells by suppressing cancer cell proliferation, invasion, increasing cisplatin chemosensitivity and inhibiting in vivo tumor growth. Hsa-miR-214-3p was confirmed to directly bind XIST, and inversely downregulated in XIST-upregulated EOC cells. In EOC cells with XIST upregulation, secondary lentiviral transduction successfully upregulated hsa-miR-214-3p expression. Subsequently, hsa-miR-214-3p upregulation functionally reversed the anticancer effects of XIST-upregulation in EOC. CONCLUSION: Upregulation of lncRNA XIST may suppress EOC development, possibly through sponging effect to induce hsa-miR-214-3p downregulation.
Cell Line ; Cell Proliferation ; Cisplatin ; Down-Regulation* ; Humans ; MicroRNAs ; Neoplasm Invasiveness ; Ovarian Neoplasms* ; RNA, Long Noncoding* ; Up-Regulation*

Objective To assess the clinical effectiveness and safety of relinqing pharmaceutical preparations for the treatment of uncomplicated urinary tract infection(UTI). Methods The genitourinary infection, urinary tract infection, pyelonephritis, cystitis, stranguria and urethritis were used as key words to search at CNKI,VIP,SinoMed,PubMed,Wan Fang and Cochrane Library Databases up to April 2015. Data of randomised controlled trials (RCTs) comparing treatments using relinqing were included in this study. The quality of the literature was evaluated by the method of Cochrane handbook 5.1.0. Data extraction was carried out independently by two authors. RevMan 5.2 software was used for Meta-analysis. Results Five RCTs were included that involved a total of 471 uncomplicated UTIs. Analysis of four studies showed a higher rates of effectiveness for uncomplicated UTI in the treatment with relinqing plus antibiotics than those of antibiotics alone [RR and 95%CI:1.15 (1.08-1.23), P<0.001]. Analysis of two studies showed a higher rates of bacterial clearance for uncomplicated UTI in the treatment with relinqing plus antibiotics than those of antibiotics alone [RR and 95% CI: 4.04 (1.78-9.16)]. Conclusion Data from five small studies suggest that relinqing as an independent intervention or in conjunction with antibiotics may be beneficial for treating uncomplicated UTIs. However, the small number and poor quality of the included studies meant that it is not possible to formulate robust conclusion on the use of relinqing for uncomplicated UTI either alone or as an adjunct to antibiotics.

Objective To review the clinical characteristics and treatment of type 1 diabetes mellitus (T1DM) in children. Methods The clinical data of 103 children with T1DM admitted to our hospital from Februry 2002 to August 2010 were retrospectively analyzed. Thirty one cases with diabetic ketoacidosis (KDA) were treated with continuous insulin pump (group A) or basal-bolus insulin therapy (group B). The differences in blood glucose control time, the rate of hypoglycemic episodes, glucose fluctuation, fasting blood glucose (FBG), 2 h postprandial blood glucose (2 hPBG), insulin dosage, the time of urine acetone bodies disappear and length of stay were compared in two groups. Results The age of 103 children with T1DM was from 38 d to 15. 33 y with an average of (8 ±3) y; most of them was 7 - 10 y (47, 45.6% ). Seventy eight children were first diagnosed accounting for 75.7%; boys accounted for 55.3% of total. Fifty one cases (49.5%) were diagnosed in winter and spring and 67 (65.2%) had infections, most of them were respiratory tract and gastrointestinal infections. Sixty two cases (60. 2% )presented as diabetic ketoacidosis at the first onset, including 4 cases (3.9%) with cerebral edema. Some patients were complicated by Hashimoto's thyroiditis, hyperthyroidism, SLE and other autoimmune diseases.Among 31 cases with ketoacidosis the FBG and PBG were decreased significantly after treatment, there were no significant differences between two groups (P ＞ 0. 05 ). Compared to group B the correction time of DKA and urine acetone bodies was shorter, and reached the targeted glucose levels more quickly, the frequency of blood fluctuation and the hypoglycemia was significantly lower, the length of stay was shorter, and the daily dose of insulin was lower in group A; the differences between two groups were statistically significant ( P ＜0. 05 or P ＜0. 01 ). Conclusions The clinical symptoms at first onset of T1 DM in children are not typical,and likely to be combined with DKA; infection may be one of the inducing factors for DKA. Continuous subcutaneous insulin infusion with pump can control the blood glucose more effectively and equably, and are convenient for use by children; so it is a better treatment option for type 1 diabetes mellitus in children.

Objective To explore the mechanism of the skin lesion induced by oxidation hair dyes Methods The effects of subjects,such as oxidation hair dyes,hydrogen peroxide (H 2O 2) and p phenylenediamine (PPD) and their mixture which were main components of oxidation hair dyes,on the proliferation of rat's keratinocytes were detected by primary culture technique of rat's keratinocytes and MTT colorimetric assay Results All of the observed groups presented a certain inhibition on proliferation of the rat's keratinocytes,except the group exposed to PPD at the lowest dose for the shorter period The OD values decreased with the increase of exposure levels and periods Dose response relationship was observed between the exposure levels and inhibition rates of cell survival(the r values after 24 h exposue: r H 2O 2 =0 981, r PPD =0 949, r PPD-H 2O 2 =0 963, r hair dyes =0 887) Conclusion The skin lesion induced by oxidation hair dyes might associated with its cytotoxicity