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MiR-221 on protective oxidative induced by selenium modified Codonopsis pilosula polysaccharide
Tao Qin1, Mengke Sun1, Yongyuan Huang2
1Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health in Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China.
International Journal of Biological Macromolecules
|August 18, 2024
Summary
MicroRNA-221 (miR-221) protects against oxidative stress induced by sCPPS5. This protection is mediated by the Keap1-Nrf2-ARE signaling pathway, highlighting miR-221
Area of Science:
- Molecular Biology
- Cellular Biology
- Biochemistry
Background:
- Oxidative stress is implicated in numerous diseases.
- MicroRNA-221 (miR-221) is known to modulate oxidative stress.
- The precise mechanism of miR-221 in sCPPS5-induced oxidative stress is not fully understood.
Purpose of the Study:
- To elucidate the protective effects of miR-221 against sCPPS5-induced oxidative stress.
- To investigate the underlying molecular mechanisms, particularly the Keap1-Nrf2-ARE signaling pathway.
Main Methods:
- Assessed oxidative stress markers: SOD, CAT, MDA, LDH, MMP, caspase-3 activity, and apoptosis.
- Utilized real-time PCR and Western blot to analyze Keap1-Nrf2-ARE pathway components.
- Evaluated effects in vivo using a mouse model.
Main Results:
- sCPPS5 treatment, particularly with miR-221 mimics, enhanced SOD and CAT expression.
- The Keap1-Nrf2-ARE signaling pathway was activated, leading to reduced MDA, MMP, caspase-3 activity, apoptosis, and LDH release.
- In vivo studies confirmed sCPPS5's ability to boost antioxidant enzymes and key signaling proteins.
Conclusions:
- miR-221 confers protection against sCPPS5-induced oxidative stress.
- This protective effect is likely mediated through the regulation of the Keap1-Nrf2-ARE signaling pathway in macrophages.
- Findings suggest a potential therapeutic role for miR-221 in managing oxidative stress-related conditions.
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