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The mitochondrial-targeted peptide SBT-20 ameliorates inflammation and oxidative stress in chronic renal failure
Lina Sun1, Haiping Xu1, Yunfei Wang2
1Department of Nephrology, Cangzhou Central Hospital, Cangzhou, Hebei Province, China.
Abstract:
Chronic renal failure (CRF) is the final outcome of the development of chronic kidney disease with different causes. Although CRF is a common clinical disease, its pathogenesis remains to be improved. SBT-20 belongs to a class of cell-permeable peptides that target the inner mitochondrial membrane, reduce reactive oxygen species (ROS), normalize electron transport chain function, and ATP generation. Our experiment was to evaluate whether SBT-20 affected the oxidative stress and inflammatory process of CRF. The levels of ROS production, mitochondrial membrane potential, NF- κB-p65, TNF-α, Drp1, and mfn2 were measured before and after SBT-20 treatment. We observed that SBT-20 treatment inhibited H2O2-induced mitochondrial ROS production. SBT-20 could also restore the mitochondrial membrane potential and reduce the elevated levels of NF-κB-p65 and TNF-α in HK-2 cells. In vivo, the renal function of CRF mice recovered after treating with SBT-20, the levels of necrotic cells and inflammation decreased, and the morphology of mitochondria recovered. The results showed that SBT-20 had a protective effect on CRF by reducing oxidative stress, inflammation progression via down-regulating of NF-κB-p65, TNF-α, and Drp1 and upregulating of Mfn2. These data support SBT-20 could be used as a potential preparation for CRF.
Insights
SBT-20, a novel peptide, effectively treats chronic renal failure (CRF) by reducing oxidative stress and inflammation. It improves mitochondrial function and renal recovery in CRF models, showing potential as a therapeutic agent.
Area of Science:
- Mitochondrial Medicine
- Nephrology
- Biochemistry
Background:
- Chronic renal failure (CRF) is a severe outcome of chronic kidney disease with incompletely understood pathogenesis.
- Mitochondrial dysfunction and oxidative stress are implicated in CRF progression.
- SBT-20 is a cell-permeable peptide targeting mitochondrial function.
Purpose of the Study:
- To investigate the therapeutic potential of SBT-20 in mitigating oxidative stress and inflammation in CRF.
- To evaluate SBT-20's effects on mitochondrial function and cellular pathways in CRF models.
Main Methods:
- Assessed reactive oxygen species (ROS) production and mitochondrial membrane potential in HK-2 cells and CRF mice.
- Measured levels of NF-κB-p65, TNF-α, Drp1, and Mfn2 before and after SBT-20 treatment.
- Evaluated renal function, cell necrosis, inflammation, and mitochondrial morphology in vivo.
Main Results:
- SBT-20 inhibited H2O2-induced mitochondrial ROS production and restored mitochondrial membrane potential in vitro.
- SBT-20 treatment reduced elevated NF-κB-p65 and TNF-α levels in HK-2 cells.
- In CRF mice, SBT-20 improved renal function, decreased necrosis and inflammation, and recovered mitochondrial morphology.
Conclusions:
- SBT-20 demonstrates a protective effect against CRF by reducing oxidative stress and inflammation.
- The mechanism involves down-regulating NF-κB-p65, TNF-α, and Drp1, and upregulating Mfn2.
- SBT-20 shows promise as a potential therapeutic preparation for CRF.
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