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Type 2 diabetic mellitus (T2DM), often accompanied by disorders of glucose and lipid metabolism, has troubled hundreds of millions of people. Xiaokeyinshui extract combination (XEC), derived from traditional Chinese medicines formula, has exerted hypoglycemic effects against T2DM. However, its mechanism of metabolic level is still unclear. In this study, a T2DM mice model, induced by a high sucrose/high fat diet combined with low-dose streptozotocin (STZ) injections, was adopted. The biochemical index was determined and a combination of metabolomics and lipidomics analyses of plasma were performed. The results showed that XEC increased secretion of insulin and level of HDL-C, decreased levels of FBG, HbA1c, TC, TG, LDL-C and repaired islet structure in diabetic mice. In addition, the metabolic profiles of plasma were analyzed and 54 potential biomarkers were screened out, mainly including carbohydrates, lipids and amino acids. These potential biomarkers were found to be correlated with the following pathways galactose metabolism, fructose and mannose metabolism, TCA cycle, arachidonic acid metabolism, glycerolipid metabolism, glycerophospholipid metabolism, sphingolipid metabolism and amino acid metabolism. In conclusion, we speculated that carbohydrate metabolism, lipid metabolism and amino acid metabolism played roles in the therapeutic mechanisms of XEC on T2DM.The long noncoding RNAs (lncRNAs) are non-coding RNAs that are more than 200 nucleotides in length, and one of several types of non-coding RNAs (ncRNAs). The lncRNAs function in diverse biological processes in normal cells, such as cellular differentiation and cell cycle regulation. There is also evidence that some aberrantly regulated lncRNAs function as oncogenes or tumor suppressor genes in various cancers. For example, TTN-AS1 is a lncRNA that binds to titin mRNA (TTN) and has pro-oncogenic effects in many cancers. Overexpression of TTN-AS1 correlates with poor prognosis in breast cancer, lung cancer, digestive system neoplasms, reproductive system cancers, and other cancers. Furthermore, increased TTN-AS1 expression correlates with more advanced pathology and tumor malignancy. In this review, we comprehensively summarize recent studies on the molecular mechanisms of TTN-AS1 regulation and the role of TTN-AS1 in the carcinogenesis and progression of numerous tumors.Osteosarcoma is rare malignancy of childhood and adolescence, with high morbidity and mortality despite accomplishment of diverse therapeutic modalities. Identification of the underlying mechanism of osteosarcoma evolution would help in better management of this rare malignancy. Lots of investigations have described abnormal regulation of long non-coding RNAs (lncRNAs) in clinical specimens of osteosarcoma and the established cell lines. This malignancy has been associated with over-expression of TUG1, LOXL1-AS1, MIR100HG, NEAT1, HULC, ANRIL and a number of other lncRNAs, while under-expression of lots of lncRNAs including LncRNA-p21, FER1L4, GAS5, LncRNA NR_136400 and LINC-PINT. Expression amounts of LUCAT1, LINC00922, SNHG12, FOXC2-AS1 and OIP5-AS1 lncRNAs have been associated with response to a number of chemotherapeutic agents. Taken together, lncRNAs are possible targets for proposing novel advanced therapeutic modalities for osteosarcoma.Twist-related protein 1 (Twist1) is a basic helix-loop-helix (bHLH) transcription factor (TF) being coded by the TWIST1 gene. This TF has a fundamental effect on the normal development and in the pathogenesis of various diseases especially cancer. Twist1 has interactions with some long non-coding RNAs and miRNAs. BAY-61-3606 order The interactions between this TF and various miRNAs such as miR-16, miR-26b-5p, miR-1271, miR-539, miR-214, miR-200b/c, miR-335, miR-10b, and miR-381 are implicated in the carcinogenic processes. TP73-AS1, LINC01638, ATB, NONHSAT101069, CASC15, H19, PVT1, LINC00339, LINC01385, TANAR, SNHG5, DANCR, CHRF, and TUG1 are among long non-coding RNAs which interact with Twist1 and participate in the carcinogenesis. This review aims at depicting the interaction between these non-coding transcripts and Twist1 and the consequence of these interactions in human neoplasms.Medicinal plants are being used for therapeutic purposes since the dawn of human civilization. The therapeutic efficacy of medicinal plants is due to the presence of wide range phytochemical constituents or secondary metabolites. The medicinal plants are traditionally used for several types of ailments. Even in those pathological conditions where other methods of treatment fail to work. Curcuma longa Linn is very common ingredient used as spice in foods as preservative and coloring material in different part of the world. It has been used as a home remedy for a variety of diseases. Curcuma longa and its isolated constituent curcumin are widely evaluated for anticancer activity. Curcumin possesses broad remedial potential due to its multi-targeting effect against many different carcinoma including leukemia, genitourinary cancers, gastrointestinal cancers and breast cancer etc. Hence, Curcumin has potential for the development of new medicine for the treatment of several diseases.Keloids are characterized by increased deposition of fibrous tissue in the skin and subcutaneous tissue following an abnormal wound healing process. Although keloid etiology is yet to be fully understood, fibroblasts are known to be key players in its development. Here we analyze the antifibrotic mechanisms of Halofuginone (HF), a drug reportedly able to inhibit the TGF-β1-Smad3 pathway and to attenuate collagen synthesis, in an in-vitro keloid model using patient-derived Keloid Fibroblasts (KFs) isolated from fibrotic tissue collected during the "Scar Wars" clinical study (NCT NCT03312166). TGF-β1 was used as a pro-fibrotic agent to stimulate fibroblasts response under HF treatment. The fibrotic related properties of KFs, including survival, migration, proliferation, myofibroblasts conversion, ECM synthesis and remodeling, were investigated in 2D and 3D cultures. HF at 50 nM concentration impaired KFs proliferation, and decreased TGF-β1-induced expression of α-SMA and type I procollagen production. HF treatment also reduced KFs migration, prevented matrix contraction and increased the metallo-proteases/inhibitors (MMP/TIMP) ratio.
My Website: https://www.selleckchem.com/products/bay-61-3606.html
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