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Published on: April 6, 2022
5-Hydroxymethylfurfural induces mice frailty through cell senescence-associated sarcopenia caused by chronic
Ting Xu1, Rong Xia2,3, Fan He1
1School of Nursing, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, PR China.
Objective:
5-Hydroxymethylfurfural (5-HMF) is an important component of air pollution, confirmed to be a risk factor for pulmonary inflammation. However, its association with general health is unknown. This article aimed to clarify the effect and mechanism of 5-HMF in the occurrence and aggravation of frailty in mice by investigating whether exposure to 5-HMF was linked to the occurrence and aggravation of mice frailty.
Methods:
Twelve male C57BL/6 mice (12-month-old, 38 ± 1 g) were randomly divided into the control group and the 5-HMF group. The 5-HMF group was treated with 5-HMF (1 mg/kg/day, respiratory exposure) for 12 months, whereas the control group was treated with equal amounts of sterile water. After the intervention, the ELISA method was used to detect the serum inflammation level of the mice, and the physical performance and frail status were evaluated using a Fried physical phenotype-based assessment tool. The differences in the body compositions were calculated from their MRI images, and the pathological changes in their gastrocnemius muscle were revealed using the H&E staining. Furthermore, the senescence of skeletal muscle cells was evaluated by measuring the expression levels of senescence-related proteins by the western blotting.
Results:
In the 5-HMF group, serum inflammatory factors IL-6, TNF-α, and CRP levels were significantly raised (p < 0.01). Mice in this group had higher frailty scores and significantly reduced grip strength (p < 0.001), slower weight gains, less WVgastrocnemius muscle masses, and lower sarcopenia indices (SI). In addition, the cross-sectional areas of their skeletal muscles were reduced, and the levels of their cell senescence-related proteins (p53, p21, p16, SOD1, SOD2, SIRT1, SIRT3) were considerably altered (p < 0.01).
Conclusion:
5-HMF may induce chronic and systemic inflammation, which in turn accelerates the progression of the frailty of mice through cell senescence.
Insights
Exposure to 5-Hydroxymethylfurfural (5-HMF), an air pollutant, accelerates frailty in mice. This occurs through induced chronic inflammation and cell senescence, impacting physical performance and muscle mass.
Area of Science:
- Environmental Health
- Toxicology
- Gerontology
Background:
- 5-Hydroxymethylfurfural (5-HMF) is an air pollutant linked to pulmonary inflammation.
- The general health effects of 5-HMF, particularly concerning frailty, remain largely unknown.
- Investigating the role of environmental factors like 5-HMF in age-related conditions is crucial.
Purpose of the Study:
- To determine the effect of 5-HMF exposure on the development and progression of frailty in a mouse model.
- To elucidate the underlying mechanisms by which 5-HMF influences frailty, focusing on inflammation and cell senescence.
Main Methods:
- Male C57BL/6 mice were exposed to 5-HMF (1 mg/kg/day) or sterile water for 12 months.
- Evaluated frailty using Fried physical phenotype assessment, grip strength, and body composition analysis (MRI).
- Assessed serum inflammatory markers (ELISA), gastrocnemius muscle pathology (H&E staining), and skeletal muscle cell senescence markers (Western Blot).
Main Results:
- 5-HMF exposure significantly increased serum inflammatory factors (IL-6, TNF-α, CRP) in mice.
- Mice exposed to 5-HMF exhibited higher frailty scores, reduced grip strength, and decreased muscle mass and skeletal muscle cross-sectional area.
- Altered expression of senescence-related proteins (p53, p21, p16, SOD1, SOD2, SIRT1, SIRT3) was observed in skeletal muscle cells.
Conclusions:
- 5-Hydroxymethylfurfural (5-HMF) exposure induces chronic systemic inflammation in mice.
- This inflammation accelerates frailty progression, likely mediated by promoting cell senescence in skeletal muscle.
- 5-HMF poses a potential risk factor for age-related frailty and associated physiological decline.
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