Naproxen attenuates osteoarthritis progression through inhibiting the expression of prostaglandinl-endoperoxide synthase 1.

OBJECTIVE: This study aims to test the effect of naproxen treatment and the biological target of naproxen for treating osteoarthritis (OA). METHODS: Differentially expressed genes (DEGs) in OA synovial tissues and normal counterparts were analyzed by messenger RNA microarray analysis. R package (weighted gene coexpression network analysis) was used to divide DEGs into several modules and determine the hub genes in each module. The expression level of prostaglandin-endoperoxide synthase 1 ( PTGS1) in OA synovial cells and tissues was verified by a quantitative real-time polymerase chain reaction and western blot. Transwell assay evaluated the numbers of cell migration and invasion. Furthermore, Safranin O and fast green staining and hematoxylin and eosin staining were performed on joints from anterior cruciate ligament transection mice. RESULTS: Microarray analysis determined PTGS1 was the hub gene in the black module, which was overexpressed in OA synovial cells and tissues compared with normal synovial cells. OA synovial cells transfected with sh-PTGS1 showed downregulation of PTGS1. After treatment with naproxen, the expression of PTGS1 sharply decreased in the OA group. The migration and invasion of OA synovial cells increased, whereas the cell apoptosis rate decreased when PTGS1 was overexpressed. However, the cell migration and invasion decreased, whereas cells apoptosis increased when it was treated with naproxen. Naproxen could also influence the expression level of six OA-related genes: LUBRICIN, matrix metalloproteinase 13 (MMP-13), cyclooxygenase-2 (COX-2), ACAN, COL2A1, and COL1A1. CONCLUSION: We validated that naproxen could suppress the expression of PTGS1 in synovial cells. Moreover, naproxen could inhibit the migration/invasion ability of OA synoviocytes and promote the apoptosis rate OA synoviocytes.

Association between dietary patterns and depressive symptoms among middle-aged adults in China in 2016-2017.

The purpose of this study was to explore the associations of dietary patterns with depressive symptoms in middle-aged Chinese adults. The cross-sectional study participants were 1360 Chinese adults (45-59 years, 659 males and 701 females) who participated in a Health Survey at the time of periodic checkup. Dietary intakes were assessed via a semi-quantitative food frequency questionnaire (FFQ). Binary logistic regression analysis was used to estimate odds ratio(OR) and 95% confidence interval(CI) for depressive symptoms according to quartiles of each dietary pattern score. Four major dietary patterns were identified by factor analysis: traditional Chinese, Western, grains-vegetables and high-salt patterns. After controlling for potential confounders, participants in the highest quartile of the Western pattern scores had greater odds of depressive symptoms than those in the lowest quartile. In contrast, participants in the highest quartile of the grains-vegetables pattern had lower odds of depressive symptoms than those in the lowest quartile. Nevertheless, no significant associations were observed between the traditional Chinese and high-salt patterns and the risk of depressive symptoms, even after adjusting for potential confounders. The findings indicate that the Western pattern is associated with an increased risk, and the grains-vegetables pattern is associated with a reduced risk of depressive symptoms.

An LC-MS/MS method for simultaneous determination of hosenkoside A and hosenkoside K from Semen Impatientis in rat plasma and its application to a pharmacokinetic study.

A rapid and sensitive liquid chromatography tandem mass spectrometry (LC-MS/MS) method was developed and validated for the simultaneous determination of two baccharane glycosides (hosenkoside A and hosenkoside K) of total saponins of Semen Impatientis in rat plasma using mogroside V as the internal standard (IS). The analytes were separated using a C18 RP Agilent XDB column (1.8 µm, 50 × 2.1 mm i.d.) and detection of the compounds was done using a TSQ Quantum triple quadrupole mass spectrometer coupled with a negative electrospray ionization source under selection reaction monitoring mode. According to the US Food and Drug Administration guidelines, the established method was fully validated and the results were proved within acceptable limits. The lower limits of quantification of both analytes were 5 ng/mL. The validated method was successfully applied to a pharmacokinetic study of orally administered the total saponins of Semen Impatientis in rats.

GLIPR1 inhibits the proliferation and induces the differentiation of cancer-initiating cells by regulating miR-16 in osteosarcoma.

Osteosarcoma is a common, highly malignant and metastatic bone cancer. Elucidation of the molecular mechanisms of osteosarcoma may further help us to understand the pathogenesis of the disease, and offer novel targets for effective therapies. Human glioma pathogenesis-related protein 1 (GLIPR1) has been found to be downregulated in human cancers. However, its roles have not been reported in osteosarcoma. In the present study, we demonstrated that GLIPR1 protein was downregulated in osteosarcoma. Its overexpression inhibited the proliferation, migration and invasion and induced the differentiation of cancer-initiating cells (CICs) in osteosarcoma. Moreover, GLIPR1 overexpression upregulated miR-16 in osteosarcoma cells. The upregulation suppressed proliferation, migration and invasion as well as induced differentiation of CICs in osteosarcoma. Thus, we conclude that GLIPR1 inhibited the proliferation, migration and invasion and induced the differentiation of CICs by regulating miR-16 in osteosarcoma. The present study provides direct evidence that GLIPR1 is a bona fide tumor suppressor and identified GLIPR1 and miR-16 as key components for regulating the proliferation, migration, invasion and CICs in osteosarcoma.