Grain-sized moxibustion at Zusanli (ST36) has a significant therapeutic effect on age-related renal injury in naturally aging mice by inhibiting the PI3K/AKT/NF-κB signaling pathway, thereby reducing inflammatory factor release and mitigating oxidative stress injury.
Key Findings
Results
Grain-sized moxibustion at ST36 improved renal histopathology and ameliorated age-related renal dysfunction in aged mice.
Design: young (3-month-old), old (21-month-old mice maintained until 24 months), and GS-Moxi group (21-month-old mice treated at ST36 for 3 months), all male mice.
Renal function was assessed by serum creatinine and blood urea nitrogen; tissue was assessed by periodic acid-Schiff and Masson's trichrome staining.
The abstract states GS-Moxi 'significantly improved renal histopathological features and ameliorated age-related renal dysfunction.' Specific effect sizes and p-values are not given in the abstract.
Results
GS-Moxi attenuated the upregulation of fibrosis markers and cellular senescence markers in aging kidneys.
Senescence markers examined were p16, p21, and senescence-associated β-galactosidase (SA-β-gal).
Fibrosis was evaluated with Masson's trichrome staining and fibrosis markers.
The abstract reports attenuation of the age-related upregulation but gives no numeric values.
Results
GS-Moxi mitigated oxidative stress alterations in aging kidneys.
Oxidative stress markers measured were superoxide dismutase (SOD) and malondialdehyde (MDA).
The abstract lists these markers as attenuated by GS-Moxi in the aging kidney.
Direction of change for each marker is not specified in the abstract.
Results
GS-Moxi reduced inflammatory cytokines in aging kidneys.
Cytokines assessed: TNF-α, IL-6, and IL-1β.
Upregulation of these cytokines in aging kidneys was attenuated by GS-Moxi.
The authors conclude that moxibustion reduces the release of inflammatory factors.
Results
Transcriptomic analysis identified the PI3K/Akt signaling pathway as a critical regulatory pathway modulated by GS-Moxi.
RNA sequencing was followed by gene set enrichment analysis (GSEA) and KEGG pathway enrichment analysis.
Both analyses pointed to PI3K/Akt signaling as a key pathway.
Results
Western blotting and immunohistochemistry confirmed that GS-Moxi modulates the PI3K/AKT/NF-κB pathway in the aging kidney.
Protein-level validation used Western blotting and IHC.
The authors conclude GS-Moxi acts by inhibiting PI3K/AKT/NF-κB signaling.
Specific protein fold-changes are not reported in the abstract.
What This Means
This study tested whether a form of moxibustion, a traditional Chinese medicine technique that involves burning small amounts of herb on the skin, could protect the kidneys from aging. Male mice that were naturally aged to 21 months received grain-sized moxibustion at an acupuncture point called Zusanli (ST36) for 3 months. They were compared with untreated old mice (up to 24 months) and young 3-month-old mice.
The treated aged mice had better kidney tissue structure and better kidney function measures (creatinine and blood urea nitrogen) than untreated old mice. They also showed lower levels of markers of fibrosis (scarring), cellular senescence (cells that stop dividing with age), oxidative stress, and inflammatory signals such as TNF-α, IL-6, and IL-1β. Gene activity analysis and protein tests suggested that these effects were linked to reduced activity of the PI3K/AKT/NF-κB signaling pathway, which is involved in inflammation.
This research suggests that moxibustion at ST36 may reduce age-related kidney damage in mice by dampening inflammation and oxidative stress. The findings come from a mouse study, so they do not show that the same effects occur in people. The abstract also gives no numerical effect sizes, so the magnitude of the benefit cannot be judged from it.
Hui X, Li Q, Yutong Q, Chang L, Zhenchen L, Qi M, et al.. (2026). Grain-sized moxibustion attenuates renal dysfunction and inflammation in naturally aging micethe phosphatidylinositol 3-kinase/protein kinase B/nuclear factor-κB pathway.. Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan. https://doi.org/10.19852/j.cnki.jtcm.2026.05.006