Journal: Diabetes, Metabolic Syndrome and Obesity

Article Title: Irisin Ameliorates Renal Tubulointerstitial Fibrosis by Regulating the Smad4/β-Catenin Pathway in Diabetic Mice

doi: 10.2147/dmso.s407734

Figure Lengend Snippet: Figure 2 Irisin may be involved in the progression of DKD through TGFBR2. (A) Expression of FNDC5 gene at mRNA level. (B) Expression of TGF-β1 gene at mRNA level. (C) Expression of TGFBR2 gene at mRNA level. (D) Red fluorescent-labeled TGFBR2 and green fluorescent-labeled irisin co-localized on the cell membrane of HK-2 cells grown in high glucose. Values are expressed as mean ± SD. **p < 0.01 vs healthy group, ***p < 0.001 vs healthy group.

Article Snippet: The plasmid overexpressing FNDC5 gene (NM-153756) was purchased from OriGene Technologies.

Techniques: Expressing, Labeling, Membrane

Journal: Diabetes, Metabolic Syndrome and Obesity

Article Title: Irisin Ameliorates Renal Tubulointerstitial Fibrosis by Regulating the Smad4/β-Catenin Pathway in Diabetic Mice

doi: 10.2147/dmso.s407734

Figure Lengend Snippet: Figure 5 Irisin restored changes in biochemical markers and renal function deterioration in diabetic mice. (A–C) After completing the FNDC5 overexpression plasmid therapy, the mice were put to death at 24 weeks and the animals were split up into the control, DM, DM+Vector, and DM+FNDC5 groups. Data on body weight, kidney weight, and the ratio of kidney weight/body weight were gathered. (D–F) 24 h urinary protein levels, Scr and TC were obtained from four different groups. (G) HE, PAS, and Masson trichrome staining in four sets of renal tissue sections are shown in example pathological images. Each experiment was carried out separately and at least three times. Values are expressed as mean ± SD. **p < 0.01 vs Control group, ***p < 0.001 vs Control group, #p< 0.05 vs DM group, ##p < 0.01 vs DM group.

Article Snippet: The plasmid overexpressing FNDC5 gene (NM-153756) was purchased from OriGene Technologies.

Techniques: Over Expression, Plasmid Preparation, Control, Staining

Journal: Diabetology & Metabolic Syndrome

Article Title: Irisin regulates integrin αvβ5/FAK/ERK to inhibit neutrophil extracellular traps formation and reduce pancreatic beta-cells pyroptosis in type 2 diabetes mellitus

doi: 10.1186/s13098-025-01852-z

Figure Lengend Snippet: Pyroptosis induced by NETs was regulated by NLRP1. A . Western blotting was performed to detect the expression of related proteins in pyroptosis in Min6 cells with NLRP1 knocked down; B . ELISA was used to detect the LDH, IL-1βand IL-18; C - D . Flow cytometry was used to detect pyroptosis in NLRP1 knocked down Min6 cells induced by NETs; N = 3, * P < 0.05, ** P < 0.01

Article Snippet: Mouse Irisin ELISA kit (E-EL-M2743), LDH ELISA kit (E-EL-M0419), IL-18 ELISA kit (E-EL-M0730) were purchased from Elabscience.

Techniques: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Flow Cytometry

Journal: Diabetology & Metabolic Syndrome

Article Title: Irisin regulates integrin αvβ5/FAK/ERK to inhibit neutrophil extracellular traps formation and reduce pancreatic beta-cells pyroptosis in type 2 diabetes mellitus

doi: 10.1186/s13098-025-01852-z

Figure Lengend Snippet: Pyroptosis induced by NETs was regulated by STING/IRE1α. A . ELISA was used to detect the LDH, IL-1β and IL-18; B - C . Western blotting was performed to detect the expression of related proteins in pyroptosis in Min6 cells with C-176 added; D - E . Flow cytometry was used to detect pyroptosis in Min6 cells with C-176 added induced by NETs; N = 3, * P < 0.05, ** P < 0.01

Article Snippet: Mouse Irisin ELISA kit (E-EL-M2743), LDH ELISA kit (E-EL-M0419), IL-18 ELISA kit (E-EL-M0730) were purchased from Elabscience.

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Flow Cytometry

Journal: Frontiers in aging neuroscience

Article Title: PGC-1α or FNDC5 Is Involved in Modulating the Effects of Aβ 1-42 Oligomers on Suppressing the Expression of BDNF, a Beneficial Factor for Inhibiting Neuronal Apoptosis, Aβ Deposition and Cognitive Decline of APP/PS1 Tg Mice.

doi: 10.3389/fnagi.2017.00065

Figure Lengend Snippet: FIGURE 2 | The Aβ1−42 oligomers suppressed the expression of BDNF through a PGC-1α- and FNDC5-dependent mechanism. (A,B) The n2a cells were treated with Aβ oligomers (1 ng/ml) for 48 h. (C,D) In select experiments, the n2a cells were transfected with either PGC-1α or FNDC5 cDNA for 48 h. (E) In separate experiments, the n2a cells were transfected with either PGC-1α or FNDC5 cDNA before the treatment with Aβ oligomers for 48 h. The mRNA and protein levels of BDNF, PGC-1α and FNDC5 were determined by qRT-PCR and western blots, respectively. GAPDH and β-actin served as the internal controls. The data represent the means ± S.E. of three times experiments. *p < 0.05 compared with vehicle-treated or vector-transfected controls. #p < 0.05 compared with Aβ-treated alone.

Article Snippet: PGC1α or FNDC5 cDNA plasmids were obtained from Origene Technologies (Rockville, MD, USA) and subcloned into the pCMV6-XL vector.

Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Plasmid Preparation

Journal: Frontiers in aging neuroscience

Article Title: PGC-1α or FNDC5 Is Involved in Modulating the Effects of Aβ 1-42 Oligomers on Suppressing the Expression of BDNF, a Beneficial Factor for Inhibiting Neuronal Apoptosis, Aβ Deposition and Cognitive Decline of APP/PS1 Tg Mice.

doi: 10.3389/fnagi.2017.00065

Figure Lengend Snippet: FIGURE 3 | Elevating the levels of PGC-1α, FNDC5 and BDNF partially protected neurons from Aβ1−42 oligomer-induced apoptosis. (A,B) The neurons were incubated with Aβ (1 ng/ml) in the absence or presence of transfection with either PGC-1α or FNDC5 cDNA. (C,D) In select experiments, the n2a cells were incubated with Aβ (1 ng/ml) in the absence or presence of BDNF (1 ng/ml). (A,C) The viability of neurons in different groups was determined by an MTT assay. (B,D) The apoptosis of neurons was determined by flow cytometry after staining with PI and annexin V. The data represent the means ± S. E. of three times experiments. *p < 0.05 compared with vehicle-treated or vector-transfected controls. #p < 0.05 compared with Aβ-treated alone.

Article Snippet: PGC1α or FNDC5 cDNA plasmids were obtained from Origene Technologies (Rockville, MD, USA) and subcloned into the pCMV6-XL vector.

Techniques: Incubation, Transfection, MTT Assay, Cytometry, Staining, Plasmid Preparation

Journal: Frontiers in aging neuroscience

Article Title: PGC-1α or FNDC5 Is Involved in Modulating the Effects of Aβ 1-42 Oligomers on Suppressing the Expression of BDNF, a Beneficial Factor for Inhibiting Neuronal Apoptosis, Aβ Deposition and Cognitive Decline of APP/PS1 Tg Mice.

doi: 10.3389/fnagi.2017.00065

Figure Lengend Snippet: FIGURE 5 | Signaling events involved in BDNF regulation during the course of AD development and the critical roles of BDNF in inhibiting the apoptosis of neurons, Aβ deposition and cognitive decline of the APP/PS1 Tg mice. BDNF expression was downregulated in the APP/PS1 Tg mice, and the Aβ1−42 oligomers are responsible for decreasing the expression of BDNF through a PGC-1α- and FNDC5-dependent mechanism. Reciprocally, elevating the levels of PGC-1α, FNDC5 and BDNF alleviated the effects of the Aβ1−42 oligomers on neuronal apoptosis. More importantly, BDNF treatment decreased the deposition of Aβ and reduced the cognitive decline of APP/PS1 Tg mice.

Article Snippet: PGC1α or FNDC5 cDNA plasmids were obtained from Origene Technologies (Rockville, MD, USA) and subcloned into the pCMV6-XL vector.

Techniques: Expressing