Fig. 5
PNS inhibits cardiomyocyte pyroptosis by downregulating lncRNA-ANRIL. A RT-qPCR was used to measure the ANRIL mRNA expression in model rats and injured cells. Male Sprague Dawley rats received 5/6 subtotal nephrectomy to construct a CRS4 rat model; model rats were administered intragastrically with corresponding doses of PNS (50 mg/kg d−1, 100 mg/kg d−1, and 200 mg/kg d−1); **p < 0.01 vs. sham group; ##p < 0.01 vs. model group; ^p < 0.05, ^^p < 0.01 vs. model + 50 mg/kg d−1 PNS group; &&p < 0.01 vs. model + 100 mg/kg d−1 PNS group. H9c2 cells were incubated in an atmosphere of 94% N2, 5% CO2, and 1% O2 for 4 h and treated with corresponding doses of PNS (100 μg/mL, 200 μg/mL, and 400 μg/mL); **p < 0.01 vs. control group; ##p < 0.01 vs. hypoxia group; ^p < 0.05, ^^p < 0.01 vs. hypoxia + 100 μg/mL PNS group; &&p < 0.01 vs. hypoxia + 200 μg/mL PNS group. B RT-qPCR was used to measure the ANRIL mRNA expression in H9c2 cells. H9c2 cells were incubated in an atmosphere of 94% N2, 5% CO2, and 1% O2 for 4 h and treated with VX765 and/or 400 μg/mL PNS. **p < 0.01 vs. control group; ##p < 0.01 vs. hypoxia group; ^^p < 0.01 vs. hypoxia + PNS group. C RT-qPCR measured the ANRIL mRNA expression in H9c2 cells. D Cell viability was determined by CCK-8. E LDH was measured by ELISA. F Cell apoptosis was determined by flow cytometry assay. G Western blotting was used to determine protein expression levels of NLRP3, IL-1β, TGF-β1, GSDMD-N, and caspase-1. C–G H9c2 cells were incubated in an atmosphere of 94% N2, 5% CO2, and 1% O2 for 4 h, treated with 400 μg/mL PNS, and transfected with oe-NC/oe-ANRIL. **p < 0.01 vs. control group; #p < 0.05, ##p < 0.01 vs. hypoxia group; ^p < 0.05, ^^p < 0.01 vs. hypoxia + PNS + oe-NC group. PNS: Panax notoginseng saponins; LncRNA: long non-coding RNA; ANRIL: antisense non-coding RNA in the INK4 locus (ANRIL); CCK-8: cell counting kit-8; LDH: Lactate dehydrogenase; TGF: transforming growth factor; IL: interleukin; GSDMD-N: N terminal of gasdermin D