Fibromyalgia syndrome (FMS), also known as fibromyalgia, is clinically characterized by diffuse chronic muscle and bone pain, accompanied by fatigue, sleep disturbances, depressive episodes, and cognitive and intestinal dysfunction. Due to lack of clear specific laboratory indicators and appropriate imaging examinations, FMS diagnosis is mostly based on clinical symptoms, but FMS clinical symptoms of lack specificity, and current clinical diagnostic criteria are mostly exclusive criteria, which is prone to missed diagnosis and misdiagnosis. In order to further promote the standardized diagnosis and treatment of FMS, this paper makes extensive references to laboratory-related diagnostic indexes of FMS (Tau, adiponectin, serum cathepsin S, cystatin C, serum ferritin, nitric oxide, neutrophil/lymphocyte ratio, platelet distribution width and mean platelet volume) at home and abroad, aiming to provide new ideas for early diagnosis and intervention of FMS.

OBJECTIVETo explore the effect and mechanism of rosuvastatin on tumor necrosis factor-α induced human mesenchymal stem cells (MSCs) apoptosis.

METHODHuman MSCs were treated as follows: (1) culture medium; (2) TNF-α (20 µg/ml) for 6 h; (3) rosuvastatin (20 µmol/L) for 24 h; (4) rosuvastatin (20 µmol/L) for 24 h followed by TNF-α (20 µg/ml) for 6 h; (5) TNF-α+rosuvastatin+50 nmol/L antago-miRNA; (6) TNF-α+rosuvastatin+100 nmol/L antago-miRNA. Cell survival and apoptosis were determined by MTT, TUNEL and caspase-3 activity assay. The changes of miRNA-210 in each group were detected with quantitative PCR.

RESULTTNF-α significantly induced human MSCs apoptosis in a concentration-dependent manner, and pretreatment with rosuvastatin significantly reduced MSCs apoptosis (caspase-3 assay: TNF-α+Statin group vs. TNF-α group: (1.63 ± 0.25) vs. (2.05 ± 0.36), P < 0.05). Meanwhile, TNF-α progressively reduced the expression of miRNA-210 in human MSCs in a dose-dependent manner, while the miRNA-210 expression was significantly upregulated in TNF-α+Statin group (P < 0.05). The protective effect of rosuvastatin on TNF-α induced MSCs apoptosis was largely abolished by co-treatment with 100 nmol/L antago-miRNA (TUNEL:TNF-α + Statin + antago-miR group vs. TNF-α + Statin group: (42.58 ± 6.71) % vs. (16.87 ± 9.27) %, P < 0.05).

CONCLUSIONPretreatment with rosuvastatin can significantly improve the viability of human MSCs after TNF-α injury, the protective mechanism of rosuvastatin is partly mediated through miRNA-210 up-regulation.

Apoptosis ; drug effects ; Caspase 3 ; Cell Survival ; Fluorobenzenes ; pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Mesenchymal Stromal Cells ; drug effects ; MicroRNAs ; pharmacology ; Pyrimidines ; pharmacology ; Rosuvastatin Calcium ; Sulfonamides ; pharmacology ; Tumor Necrosis Factor-alpha ; drug effects ; Up-Regulation