Figures & data
Figure 1. Ginsenoside Rg1 protected Podocytes from IL1β-induced inflammation. (A–D) RT-PCR analysis indicated Ginsenoside Rg1 attenuated IL1β-induced expression of inflammatory cytokines, (n = 6). **p < .01; ***p < .001; versus respective control.
Figure 2. Ginsenoside Rg1 attenuated IL1β-induced apoptosis and activated NRF2 signalling. (A) Western blot analysis indicated Ginsenoside Rg1 protected podocytes from IL1β-induced apoptosis, (n = 3). (B–D) Ginsenoside Rg1 activated NRF2 signalling and inhibited IL1β-stimulated ERK and P38 pathway (n = 3). *p < .05; **p < .01; versus respective control.
Figure 3. NRF2 inhibitor ML385 inhibited NRF2 signalling and promoted IL-1β-induced apoptosis in podocytes. (A–C) ML385 inhibited NRF2 signalling and re-activated ERK and P38 signalling pathway (n = 3). (D) ML385 diminished the inhibitory effect of Ginsenoside Rg1 on attenuating apoptosis in podocytes (n = 3). *p < .05; **p<.01; versus respective control.
Figure 4. NRF2 inhibitor ML385 abrogated anti-inflammatory effect of Ginsenoside Rg1 on podocytes. (A–D) ML385 eliminated inhibitory effect of Ginsenoside Rg1 on attenuating inflammation in podocytes (n = 6). *p < .05; **p < .01; ***p < .001; versus respective control.
Figure 5. Rg1 improved anti-GBM glomerulonephritis induced inflammation in vivo. (A) Immunostaining showed that anti-GBM glomerulonephritis model was successfully constructed. (B–E) Rg1 decreased expression of inflammatory cytokines in anti-GBM glomerulonephritis model via RT-PCR analysis (n = 6). (F–I) Rg1 attenuated immune response induced expression of total IgG, anti-GBM, CD163 and CD206. *p < .05; **p < .01; ***p < .001; versus respective control.
Figure 6. Ginsenoside Rg1 showed beneficial effect on inhibiting apoptosis and activated NRF2 signalling in mice. (A) Ginsenoside Rg1 protected renal function from apoptosis (n = 3). (B–D) Ginsenoside Rg1 activated NRF2 signalling and inhibited ERK and P38 pathway in vivo (n = 3). *p < .05; **p < .01; versus respective control.
