Objective: To explore the mechanism by which ghrelin regulates insulin sensitivity through modulation of miR-455-5p in hepatic cells. Methods: HepG2 cells were treated with or without DAG (1 μM). Glucose consumption,...Objective: To explore the mechanism by which ghrelin regulates insulin sensitivity through modulation of miR-455-5p in hepatic cells. Methods: HepG2 cells were treated with or without DAG (1 μM). Glucose consumption, intracellular glycogen content, phosphorylation of PI3K and Akt stimulated by insulin, expression of miR-455-5p, as well as IGF-1R protein level were analyzed. In addition, bioinformatic analysis, dual luciferase reporter assay, miR- 455-5p mimic or inhibitor treatment was conducted to investigate the molecular mechanisms. Results: High glucose treatment upregulated miR-455-5p expression but reduced glucose consumption and glycogen content. DAG reversed the effect of high glucose on glucose metabolism, increased protein level of IGF-1R and phosphorylation of PI3K/Akt stimulated by insulin, as well as downregulated miR-455-5p expression. Bioinformatic analysis indicated IGF-1R was the target of miR-455-5p. Dual luciferase reporter assay, as well as transfection with miR-455-5p mimic/inhibitor confirmed that DAG activated IGF-1R/PI3K/Akt signaling via inhibiting miR-455-5p. Conclusion: DAG improves insulin resistance via miR-455-5p- mediated activation of IGF-1R/PI3K/Akt system, suggesting that suppression of miR-455-5p or activation of DAG may be potential targets for T2DM therapy.展开更多
Aim To investigate the protective effects of gentiopicroside （GPS） on acute alcohol-induced fatty liver.Methods Mice were treated with ethanol （5 g · kg^-11 of body weight） by gavage every 12 h for a total of...Aim To investigate the protective effects of gentiopicroside （GPS） on acute alcohol-induced fatty liver.Methods Mice were treated with ethanol （5 g · kg^-11 of body weight） by gavage every 12 h for a total of three do- ses to induce acute fatty liver. GPS （40 or 80 mg · kg^-1 ） was garaged with ethanol simultaneously for three doses. Administration of GPS significantly prevented the increases of serum ALT and AST caused by ethanol, as well as se- rum and hepatic TG. Results GPS could significantly prevent ethanol-induced hepatic steatosis and necrosis by H＆E and Oil Red O staining. GPS also significantly inhibited lipogenic genes including sterol regulatory element binding transcription factor 1 （ SREBP-1 ）, fatty acid synthase （FASN） and acetyl-CoA carboxylase （ACC） in eth- anol-treated mice. Additionally, GPS possessed the ability to prevent ethanol-induced acute liver steatosis, possibly through inducing the phosphorylation of AMP-activated protein kinase （AMPK） and liver kinase B1 （LKB1）. Af- ter treatment with GPS, peroxisome proliferator-activated receptor eL （PPARoL） protein expression in mouse liver was recovered as that level of normal mice. Ethanol treatment evoked P2X7r and caspase-1 protein expression, while GPS significantly suppressed those protein expressions. GPS may be developed as a potential therapeutic can- didate for ethanol-induced hepatic steatosis and inflammation.展开更多
We propose a rational quantum deformed nonlocal currents in the homogeneous space SU(2)k/U(1), and in terms of it and a free boson field a representation for the Drinfeld currents of Yangian double at a general level ...We propose a rational quantum deformed nonlocal currents in the homogeneous space SU(2)k/U(1), and in terms of it and a free boson field a representation for the Drinfeld currents of Yangian double at a general level k = c is obtained. In the classical limit h → 0, the quantum nonlocal currents become SU(2)k parafermion, and the realization of Yangian double becomes the parafermion realization of SU(2)k current algebra.展开更多
基金Changshu Science and Technology Plan(Social Development)Project(No.CS202130)Key Project of Changshu No.2 People’s Hospital(No.CSEY2021007)。
文摘Objective: To explore the mechanism by which ghrelin regulates insulin sensitivity through modulation of miR-455-5p in hepatic cells. Methods: HepG2 cells were treated with or without DAG (1 μM). Glucose consumption, intracellular glycogen content, phosphorylation of PI3K and Akt stimulated by insulin, expression of miR-455-5p, as well as IGF-1R protein level were analyzed. In addition, bioinformatic analysis, dual luciferase reporter assay, miR- 455-5p mimic or inhibitor treatment was conducted to investigate the molecular mechanisms. Results: High glucose treatment upregulated miR-455-5p expression but reduced glucose consumption and glycogen content. DAG reversed the effect of high glucose on glucose metabolism, increased protein level of IGF-1R and phosphorylation of PI3K/Akt stimulated by insulin, as well as downregulated miR-455-5p expression. Bioinformatic analysis indicated IGF-1R was the target of miR-455-5p. Dual luciferase reporter assay, as well as transfection with miR-455-5p mimic/inhibitor confirmed that DAG activated IGF-1R/PI3K/Akt signaling via inhibiting miR-455-5p. Conclusion: DAG improves insulin resistance via miR-455-5p- mediated activation of IGF-1R/PI3K/Akt system, suggesting that suppression of miR-455-5p or activation of DAG may be potential targets for T2DM therapy.
文摘Aim To investigate the protective effects of gentiopicroside （GPS） on acute alcohol-induced fatty liver.Methods Mice were treated with ethanol （5 g · kg^-11 of body weight） by gavage every 12 h for a total of three do- ses to induce acute fatty liver. GPS （40 or 80 mg · kg^-1 ） was garaged with ethanol simultaneously for three doses. Administration of GPS significantly prevented the increases of serum ALT and AST caused by ethanol, as well as se- rum and hepatic TG. Results GPS could significantly prevent ethanol-induced hepatic steatosis and necrosis by H＆E and Oil Red O staining. GPS also significantly inhibited lipogenic genes including sterol regulatory element binding transcription factor 1 （ SREBP-1 ）, fatty acid synthase （FASN） and acetyl-CoA carboxylase （ACC） in eth- anol-treated mice. Additionally, GPS possessed the ability to prevent ethanol-induced acute liver steatosis, possibly through inducing the phosphorylation of AMP-activated protein kinase （AMPK） and liver kinase B1 （LKB1）. Af- ter treatment with GPS, peroxisome proliferator-activated receptor eL （PPARoL） protein expression in mouse liver was recovered as that level of normal mice. Ethanol treatment evoked P2X7r and caspase-1 protein expression, while GPS significantly suppressed those protein expressions. GPS may be developed as a potential therapeutic can- didate for ethanol-induced hepatic steatosis and inflammation.
文摘We propose a rational quantum deformed nonlocal currents in the homogeneous space SU(2)k/U(1), and in terms of it and a free boson field a representation for the Drinfeld currents of Yangian double at a general level k = c is obtained. In the classical limit h → 0, the quantum nonlocal currents become SU(2)k parafermion, and the realization of Yangian double becomes the parafermion realization of SU(2)k current algebra.
