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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
Molecular mechanisms of hydrogen sulfide against uremic accelerated atherosclerosis through cPKCβII/Akt signal
Ruifang Xiong1, Xiangxue Lu1, Jinghong Song1
1Department of Blood Purification, Beijing Chao-Yang Hospital, Capital Medical University, No. 8 Gongti South Road, Chaoyang District, Beijing, 100020, China.
Insights
Hydrogen sulfide (H2S) protects against uremia accelerated atherosclerosis (UAAS) by regulating the conventional protein kinase C βII (cPKCβII)/Akt pathway. Imbalances in the cystathionine-γ-lyase (CSE)/H2S system contribute to UAAS by affecting endothelial nitric oxide synthase (eNOS) expression.
Area of Science:
- Biochemistry
- Cardiovascular Research
- Nephrology
Background:
- Cardiovascular disease (CVD) is a major cause of death in hemodialysis patients.
- The role of hydrogen sulfide (H2S) and the cPKCβII/Akt pathway in atherosclerosis is debated.
Purpose of the Study:
- To investigate the protective mechanism of H2S against uremia accelerated atherosclerosis (UAAS).
- To elucidate the role of the cPKCβII/Akt signaling pathway in UAAS.
Main Methods:
- An animal model of UAAS was established using ApoE-/- mice with 5/6 nephrectomy and a high-fat diet.
- Mice were treated with L-cysteine, sodium hydrosulfide (NaHS), or propargylglycine (PPG).
- Western blot analysis was used to assess cPKCβII activation, Akt phosphorylation, and eNOS expression in mouse aortas.
Main Results:
- UAAS mice showed increased cPKCβII translocation and decreased Akt phosphorylation and eNOS expression compared to controls.
- L-cysteine and NaHS treatments reduced cPKCβII translocation and preserved Akt phosphorylation and eNOS expression.
- PPG treatment exacerbated cPKCβII translocation and decreased Akt phosphorylation and eNOS expression.
Conclusions:
- The endogenous cystathionine-γ-lyase (CSE)/H2S system protects against UAAS via the cPKCβII/Akt pathway.
- Imbalances in the CSE/H2S system may promote UAAS by altering eNOS expression through the cPKCβII/Akt signaling pathway.
Background:
Cardiovascular disease is the most common complication and leading cause of death in maintenance hemodialysis patients. The protection mechanism of hydrogen sulfide (H2S) and the specific role of conventional protein kinase C βII (cPKCβII)/Akt signaling pathway in the formation of atherosclerosis is still controversial.
Methods:
8-week-old male ApoE-/- mice were treated with 5/6 nephrectomy and high-fat diet to make uremia accelerated atherosclerosis (UAAS) model. Mice were divided into normal control group (control group), sham operation group (sham group), UAAS group, L-cysteine group (UAAS+L-cys group), sodium hydrosulfide group (UAAS+NaHS group), and propargylglycine group (UAAS+PPG group). Western blot was used to detect cPKCβII activation, Akt phosphorylation and endothelial nitric oxide synthase (eNOS) expression in mice aorta.
Results:
The membrane translocation of cPKCβII in UAAS group was higher than sham group, and L-cys or NaHS injection could suppress the membrane translocation, but PPG treatment resulted in more membrane translocation of cPKCβII (P < 0.05, n = 6 per group). Akt phosphorylation and the eNOS expression in UAAS group was lower than sham group, and L-cys or NaHS injection could suppress the degradation of Akt phosphorylation and the eNOS expression, but PPG treatment resulted in more decrease in the Akt phosphorylation and the eNOS expression (P < 0.05, n = 6 per group).
Conclusion:
Endogenous cystathionine-γ-lyase (CSE)/H2S system protected against the formation of UAAS via cPKCβII/Akt signal pathway. The imbalance of CSE/H2S system may participate in the formation of UAAS by affecting the expression of downstream molecule eNOS, which may be mediated by cPKCβII/Akt signaling pathway.
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