Reversal of Chronic Stress-Induced Inflammaging by Bazi Bushen Formula Through AMPK-Sirtuins Axis Activation and Myeloid Reset.
Abstract
Chronic stress potentially accelerates aging and increases age-related disease risk. However, the underlying mechanisms and organ specificity remain unclear. Utilizing a 12-month unpredictable chronic mild stress (UCMS) mouse model, we revealed chronic stress significantly exacerbates systemic inflammation, causing widespread tissue damage and lifespan shortening. Integrated single-cell RNA sequencing analysis of multiple tissues suggests a common feature of lymphocyte reduction and myeloid cell expansion. The lungs and kidneys exhibited pronounced stress responses, including epigenetic dysregulation and mitochondrial dysfunction. Both β-nicotinamide mononucleotide (NMN) and compound medicine Bazi Bushen (BZBS) effectively alleviate the UCMS-induced aging phenotypes. BZBS restores immune system homeostasis and reduces stress/inflammation levels in various tissues. Bioactive compounds from BZBS constituents
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Research summary
Bazi Bushen Formula reverses chronic stress-induced inflammaging and extends lifespan by activating the AMPK-Sirtuins axis and resetting myeloid cells. The paper is relevant because it investigates the mechanistic pathways (AMPK/Sirtuins) underlying stress-accelerated aging and demonstrates that a specific intervention can reverse these aging phenotypes and extend lifespan in a chronic stress model, addressing the root causes of accelerated aging rather than just treating symptoms.
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