Fig 2: Effect of PTP1B knockdown in SH-SY5Y on PTP1B expression and neuroprotective effect against 6-OHDA damage. (a) SH-SY5Y cells were transfected with siRNAs by LipofectAMINE PlusReagent for 3 h and incubated with new medium overnight. Western blotting for PTP1B of the control (negative control), 6-OHDA (negative control), control (positive control), 6-OHDA (positive control), control (PTP1B siRNA), and 6-OHDA (PTP1B siRNA) groups is shown. Data are presented as mean ± SEM, and each value contains three replicates and three samples. *Significantly different from the control (negative control) group. (b) SH-SY5Y cells were transfected with siRNAs by LipofectAMINE PlusReagent for 3 h and incubated with new medium overnight. Cell viability of the control (negative control), 6-OHDA (negative control), control (positive control), 6-OHDA (positive control), control (PTP1B siRNA), and 6-OHDA (PTP1B siRNA) groups is measured. Data are presented as mean ± SEM, and each value contains three replicates and three samples. *Significantly different from the control (negative control) group. #Significantly different from the 6-OHDA (negative control) group.

Fig 3: Schematic diagram of the proposed mechanisms underlying the protective effects of FA on oxidative stress, inflammation in macrophages and HSC activation during liver fibrosis. FA ameliorated CCl4-induced oxidative stress in hepatocytes, relieved LPS-induced inflammation in macrophages and alleviated TGF-ß-induced fibrotic response in HSCs. The potential mechanism was that FA directly bound to and inhibited the activity of PTP1B, eventually leading to the phosphorylation of AMPK.

Fig 4: Augmentation of plasma inflammatory factor levels and increased glomerular PTP1B expression in DN patients and rats.A–C ELISA indicated that IL-1ß, TNFa and IL-6 were increased in DN patients (n = 20/group). D Haematoxylin–eosin staining (HE) of renal biopsy specimens from DN patients and control participants. E Masson staining of renal biopsy specimens from DN patients and control participants. F Immunohistochemistry (IHC) of p-p65 in renal biopsy specimens of DN patients and control participants. G IHC of PTP1B in renal biopsy specimens of DN patients and control participants. H–J ELISA indicated that IL-1ß, TNFa and IL-6 were increased in DN rats (n = 10/group). K HE of renal biopsy specimens of DN rats and control rats. L Masson staining of renal biopsy specimens of DN rats and control rats. M IHC of p-p65 in renal biopsy specimens of DN rats and control rats. N IHC of PTP1B in renal biopsy specimens of DN rats and control rats. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n = 10/group).

Fig 5: FA directly inhibits PTP1B activity but MF doesn’t affect PTP1B and AMPK signalings in different liver cells. (A) Inhibition of the catalytic activity of PTP1B by FA was shown. (B) LX-2 cells were treated with 25 µM FA for 24 h. Immunoprecipitation using monoclonal anti-PTP1B or IgG, followed by western blot analysis using rabbit polyclonal anti-p-AMPK and t-AMPK. 10% input was prepared as a positive control and ß-ACTIN was used as a loading control. (C) Chemical structures of FA and MF. (D) Representative images for the binding mode of MF and PTP1B. (E) Inhibition of the catalytic activity of PTP1B by MF was shown. (F and H) MPHs, LX-2 cells and (G) RAW cells were treated with 25 or 100 µM MF at different time points. (F-H) Representative immunoblots against p-AMPK, t-AMPK, PTP1B and ß-ACTIN were shown. One-way ANOVA with Tukey’s post-hoc tests (n = 3).