Mechanism of paraventricular nucleus H ₂ S on PERK / TXNIP / NLRP3 pathway in male spontaneously hypertensive rats

Figures

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  FIGURE 1. Effects of SAMe and GSK intervention on blood pressure, plasma NE levels, and PVN levels of H2S in SHR. (a) Changes in MAP. (b) Changes in plasma NE. (c) Changes in PVN levels of H2S. All data are expressed as a mean ± SD. n = 14 in each group for MAP and NE, n = 4 in each group for H2S. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 2. Effect of SAMe and GSK treatment on CBS expression in the PVN of SHR. (a) Immunofluorescence staining of CBS in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of CBS in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 3. Effect of SAMe and GSK treatment on p‐PERK expression in the PVN of SHR. (a) Immunofluorescence staining of p‐PERK in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of p‐PERK in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 4. Effect of SAMe and GSK treatment on TXNIP expression in the PVN of SHR. (a) Immunofluorescence staining of TXNIP in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of TXNIP in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 5. Effect of SAMe and GSK treatment on NLRP3 expression in the PVN of SHR. (a) Immunofluorescence staining of NLRP3 in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of NLRP3 in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 6. Effect of SAMe and GSK treatment on ASC expression in the PVN of SHR. (a) Immunofluorescence staining of ASC in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of ASC in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 7. Effect of SAMe and GSK treatment on Caspase‐1 expression in the PVN of SHR. (a) Immunofluorescence staining of Caspase‐1 in the rat PVN, scale bar = 50 μm. (b) Statistical graph in average absorbance of Caspase‐1 in the rat PVN. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 8. Effects of SAMe and GSK on the expression of CBS, PERK/TXNIP/NLRP3 pathway‐related proteins, and inflammatory cytokines in the PVN of SHR. (a) Protein electropherograms of CBS, p‐PERK/PERK, TXNIP, NLRP3, ASC, pro‐Caspase‐1, Caspase‐1 p20, IL‐1β, TNF‐α, and IL‐18. (b–k) Results of statistical analysis of the related proteins and inflammatory factors in the PVN of each group of rats, respectively. All data are expressed as a mean ± SD. n = 6 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 9. Effects of SAMe and GSK on the mRNA expression levels of IL‐1β, TNF‐α, and IL‐18 in the PVN of SHR. (a–c) Results of statistical analysis of mRNA levels of IL‐1β, TNF‐α, and IL‐18 in the PVN of rats in each group, respectively. All data are expressed as a mean ± SD. n = 4 in each group. SAMe (an endogenous H2S agonist), GSK (a PERK inhibitor).

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  FIGURE 10. Effects of BMS and SAMe on cell viability of PC12 cells. (a) Results of the CCK‐8 assay in PC12 cells treated with BMS at concentrations of 0, 0.1, 1, 5, 10, and 100 μM. (b) Results of the CCK‐8 assay in PC12 cells treated with SAMe at concentrations of 0, 0.1, 1, 5, 10, and 100. All data are expressed as a mean ± SD. n = 3 in each group. BMS (an NLRP3 activator), SAMe (an endogenous H2S agonist).

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  FIGURE 11. Effects of SAMe and BMS on the mRNA expression levels of NLRP3, IL‐1β, TNF‐α, and IL‐18 in PC12 cells. (a–d) Results of statistical analysis of mRNA levels of NLRP3, IL‐1β, TNF‐α, and IL‐18 in PC12 cells in each group, respectively. All data are expressed as a mean ± SD. n = 3 in each group. BMS (an NLRP3 activator), SAMe (an endogenous H2S agonist).