μ Mol / l] level decreased significantly, insulin resistance improved, fins [(51.58 ± 1.49) mu / l] and ISI (- 6.32 ± 0.11) increased significantly, and H2S concentration in pancreatic tissue [(71.48 ± 10.94) μ Mol / l] decreased significantly, and AIEP and PRSI increased.
Results there were 18 miRNAs up-regulated and 65 down regulated in skin wound tissues of diabetic rats.
The verification results of real time PCR are in good agreement with the chip detection results.
45 rats were randomly divided into diabetes (DM), DM+ sodium sulphide (NaHS) and DM+DL- propargylglycine (PAG) group, 15 rats in each group, and another normal control group.
Functional enrichment analysis showed that the differentially expressed miRNAs such as miR-31, miR-222 and mir-449a were involved in Kyoto genes and genome Encyclopedia (KEGG) signal pathways related to wound repair, such as mitogen activated protein kinase (MAPK), Wnt and notch, respectively..
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Rats in DM + NaHS group were intraperitoneally injected with NaHS [56] μ Mol / (kg · d)], PAG [50mg / (kg · d)] was injected intraperitoneally in DM + PAG group.
Conclusion H2S plays an important role in the development of diabetes mellitus by affecting insulin resistance and lipid metabolism in T2DM rats.
Results compared with the control group, FBG [(18.22 ± 3.99) mmol / l], TG [(1.54 ± 0.16) mmol / l], TC [(3.27 ± 0.38) mmol / l] and FFA [(504.68 ± 37.70) in DM group μ Mol / l] level and HOMA-IR increased (P & lt; 0.05), fins [(41.79 ± 3.43) mu / l] and ISI (- 6.57 ± 0.37) decreased, and H2S concentration in pancreatic tissue [(96.98 ± 19.44) μ The area of insulin positive cells (AIEP) and insulin positive staining rate (PRSI) decreased with the increase of mol / L (P & lt; 0.05); Compared with the DM group, after NaHS intervention, FBG[in diabetic rats (25.42 + 0.21) mmol/L], TG[(2.40 + 0.21) mmol/L], TC[(4.80 + 0.16) mmol/L], FFA[(633.96 + 25.64).
The control group and DM group were given the same volume of normal saline for 2 weeks.
Methods a T2DM model was established in 65 rats by high glucose and high-fat diet plus intraperitoneal injection of streptozotocin (STZ).
μ Mol / l] level and HOMA-IR increased more significantly, fins [(29.36 ± 2.65) mu / l] and ISI (- 6.58 ± 0.27) decreased, and H2S concentration in pancreatic tissue [(134.50 ± 12.70) μ Mol / l] increased significantly, AIEP and PRSI decreased, and the difference was statistically significant (P & lt; 0.05); After application of PAG, plasma FBG[(10.83 + 1.10) mmol/L], TG[(1.30 + 0.12) mmol/L], TC[(2.79 + 0.33) mmol/L], FFA[(383.39 + 69) in diabetic rats.
After administration, fasting blood glucose (FBG), insulin (fins), triglycerides (TG), total cholesterol (TC) and free fatty acids (FFA) were measured, and insulin resistance index (HOMA-IR) and insulin sensitivity index (ISI) were calculated; The concentration of hydrogen sulfide (H2S) in pancreatic tissue was measured, and the expression of insulin in pancreatic tissue was detected by immunohistochemical method.
After purification, fluorescent labeling and chip hybridization were carried out, and then the hybridization picture was scanned; Using software to extract data and parallel difference analysis; The chip results were verified by real-time quantitative polymerase chain reaction (real-time PCR).
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After 4 weeks, 6 rats in diabetic model rats and normal rats were taken, and the full-thickness skin excision wound was prepared on the back.
Methods male SD rats, body mass 200~250g and streptozotocin intraperitoneal injection were used to establish a diabetic rat model.
Three days after modeling, the above wound tissues were cut surgically; The total RNA was extracted with Trizol and inspected.
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Objective To observe the effects of hydrogen sulfide on insulin resistance and lipid metabolism in type 2 diabetes mellitus (T2DM) rats.
Objective to investigate the differential expression profiles of micro RNA (miRNAs) in skin tissue of diabetic rats and normal rats.
The significantly up-regulated miRNAs include rno-mir-496-5p, rno-mir-105, rno-mir-122-5p, etc; The significantly down regulated miRNAs include rnomir-196a-5p, rno-mir-134-5p, rno-mir-31-3p and so on.
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