Journal: American Journal of Transplantation

Article Title: Donor Graft Micro RNA s: A Newly Identified Player in the Development of New‐onset Diabetes After Liver Transplantation

doi: 10.1111/ajt.13984

Figure Lengend Snippet: TAC‐induced dysregulation of mi RNA s and their potential targets. (A) The expressions of let‐7a, miR‐26b, and miR‐183 were significantly increased after different concentrations of TAC treatment (5 or 20 ng/mL vs. 0 ng/mL). (B) The expressions of let‐7a, miR‐26b, and miR‐183 did not significantly change after different culture times (48 or 72 h vs. 24 h) in physiological concentrations of TAC treatment (5 ng/mL). (C) The expressions of let‐7a, miR‐26b, and miR‐183 were increased in a time‐related manner (48 or 72 h vs. 24 h) in extremely high concentrations of TAC treatment (20 ng/mL). (D) The selected glucose metabolism‐associated targets (Akt, Irs2, Gsk3, Tcf7l2, and Foxo1) of let‐7, miR‐26b, and miR‐183 were significantly decreased after TAC treatment. The protein content of p‐ AKT , AKT , IRS 2, TCF 7L2, and FoxO1 decreased after TAC treatment. HepG2 and HUH 7 cells were seeded at 2.5 × 10 5 cells per well in six‐well plates and treated with different concentrations of TAC (0, 5, or 20 ng/mL). Protein was extracted after 72 h of culture. *p < 0.05 versus control group. TAC , tacrolimus; miRNA, microRNA.

Article Snippet: The primary antibodies used were antihuman IRS2 antibody (Catalog No. bs‐0173R, 1:500, bioss, Beijing, China), antihuman AKT antibody (Catalog No. 4685, 1:2000, Cell Signaling, Danvers, MA), antihuman pAKT (Ser473) antibody (Catalog No. 4060, 1:2000, Cell Signaling), antihuman FoxO1 antibody (Catalog No. 2880, 1:1000, Cell Signaling), antihuman TCF7L2 (TCF4) antibody (Catalog No. 2565, 1:1000, Cell Signaling), and anti‐β actin antibody (Catalog No. 3700, 1:3000, Cell Signaling).

Techniques:

Journal: American Journal of Transplantation

Article Title: Donor Graft Micro RNA s: A Newly Identified Player in the Development of New‐onset Diabetes After Liver Transplantation

doi: 10.1111/ajt.13984

Figure Lengend Snippet: The glucose metabolism‐associated pathways identified by GO and KEGG pathway analysis using potential targets of microRNAs upregulated by both low‐ and high‐dose TAC

Article Snippet: The primary antibodies used were antihuman IRS2 antibody (Catalog No. bs‐0173R, 1:500, bioss, Beijing, China), antihuman AKT antibody (Catalog No. 4685, 1:2000, Cell Signaling, Danvers, MA), antihuman pAKT (Ser473) antibody (Catalog No. 4060, 1:2000, Cell Signaling), antihuman FoxO1 antibody (Catalog No. 2880, 1:1000, Cell Signaling), antihuman TCF7L2 (TCF4) antibody (Catalog No. 2565, 1:1000, Cell Signaling), and anti‐β actin antibody (Catalog No. 3700, 1:3000, Cell Signaling).

Techniques:

Journal: BMC Complementary Medicine and Therapies

Article Title: Buddleoside-rich Chrysanthemum indicum L. extract modulates macrophage-mediated inflammation to prevent metabolic syndrome induced by unhealthy diet

doi: 10.1186/s12906-024-04583-2

Figure Lengend Snippet: Primer sequence list

Article Snippet: The sections were then added with primary antibody IRS2 (R382966, Zenbio, 1:200), INS Monoclonal antibody (66198-1-Ig, Proteintech, 1:250) and Glucagon polyclonal antibody (15954-1-AP, Proteintech, 1:500) mixture overnight at 4°C.

Techniques: Sequencing

Journal: BMC Complementary Medicine and Therapies

Article Title: Buddleoside-rich Chrysanthemum indicum L. extract modulates macrophage-mediated inflammation to prevent metabolic syndrome induced by unhealthy diet

doi: 10.1186/s12906-024-04583-2

Figure Lengend Snippet: Effect of BUDE on insulin resistance in model rats. ( A , B ) Glucose tolerance test and area under the blood glucose curve. ( n = 10). ( C ) Serum fasting insulin levels. ( n = 10). ( D - E ) Insulin resistance index and insulin sensitivity index. ( n = 10). ( F ) Representative image of pancreatic immunofluorescence double staining (400×). ( n = 3). ( G ) Percentage of pancreatic islet alpha cells. ( n = 3). ( H ) Hepatic glycogen content. ( n = 10). ( I ) Hepatic insulin receptor substrate1 (IRS1), insulin receptor substrate2 (IRS2), and glucose transporter 2 (GLUT2) mRNA levels. ( n = 3). ( J ) Representative graph of pancreatic IRS2 immunofluorescence. ( n = 3). Compared with the normal group, ▲ P < 0.05, ▲▲ P < 0.01; compared with the model group, * P < 0.05, ** P < 0.01. NG: normal control group; MG: model control group; BUDE-L: BUDE low-dose (75 mg·kg − 1 ) group; BUDE-H: BUDE high-dose (150 mg·kg − 1 ) group

Article Snippet: The sections were then added with primary antibody IRS2 (R382966, Zenbio, 1:200), INS Monoclonal antibody (66198-1-Ig, Proteintech, 1:250) and Glucagon polyclonal antibody (15954-1-AP, Proteintech, 1:500) mixture overnight at 4°C.

Techniques: Immunofluorescence, Double Staining, Control

Journal: World Journal of Gastroenterology : WJG

Article Title: Ameliorative effects of lutein on non-alcoholic fatty liver disease in rats

doi: 10.3748/wjg.v21.i26.8061

Figure Lengend Snippet: Lutein supplementation improved insulin signaling in rat liver. Effects of lutein on the mRNA expression of IRS2 (A), PI3K (B), and GLUT2 (C) in rat liver (n = 4). Total RNA was extracted from rat livers using TRIzol. IRS2, PI3K, and GLUT2 expression was analyzed by Real-Time RT-PCR. β-actin mRNA was quantified as an endogenous control. IRS2, PI3K, and GLUT2 are presented as fold changes relative to the control. Effect of lutein on the protein expression of hepatic IRS2 (D), PI3K (E), and GLUT2 (F) in rats (n = 3). After the rats were treated with lutein for 45 d, hepatic lysates were prepared and immunoblotted with corresponding antibodies. Blotting with anti β-actin was used as a protein loading control. Data are expressed as the mean ± SD. aP < 0.05 vs normal diet (ND) group; cP < 0.05 vs the high-fat diet (HFD) group.

Article Snippet: After blocking, the membranes were incubated with one of the following primary antibodies overnight at 4 °C: IRS2 (Cell Signaling Technology; Cat. No. 3089), PI3K-P85 (Cell Signaling Technology; Cat. No. 4257), GLUT2 (Santa Cruz Biotechnology, Inc.; Cat. No. sc-9117), PPAR-α (abcam; Cat. No. ab8934), SIRT1 (Santa Cruz Biotechnology, Inc.; Cat. No. sc-15404), or β-actin (Sigma; Cat. No. A1978).

Techniques: Expressing, Quantitative RT-PCR, Control