| 論文作者 |
Liao, YX; Lin, S; Yang, N; Zhou, HH; Mo, XX; Wen, L; Liang, XL; King, L; Zhou, SL; Sun, YH; Shen, LH; Li, LY; Zhang, YH; He, RK; Yang, W; Liu, LG |
| 摘要 |
Background and Purpose: Dietary advanced glycation end-products (AGEs), toxic compounds abounded in ultra-processed foods (UPF), potentially caused skeletal muscle damage, which is expected to be alleviated by berries due to their bioactive polyphenol-anthocyanins. This study aims to explore the effects of dietary AGEs on skeletal muscle and whether berries, specifically European bilberry extract (EBE, with similar to 36 % anthocyanins), could protect against dietary AGEs-induced muscle damage. Methods: A prospective cohort study of 37967 UKB participants with at least one 24-h dietary recall were included. UPF were categorized by the NOVA classification system, and berries intake of participants was collected. Low muscle strength (LMS) and mass (LMM) were assessed based on the cut-off points recommended in the EWGSOP2 definition. Cox models were used to analyze the associations. Three-month-old Sprague-Dawley rats received non-baked diet, baked diet (BD), BD plus 100 mg/kg bw EBE or BD plus 200 mg/kg bw EBE for 15 months, respectively, to explore the impact of dietary AGEs and EBE on muscle. The effects of EBE and anthocyanins on the proliferation and differentiation of L6 myoblasts after AGEs exposure were also evaluated. Potential mechanisms were predicted through network pharmacology and verified by experiments. Results: After a median follow-up of 8.08 years, 3439 cases of LMS and 1984 cases of LMM were observed in this cohort. The risk of LMS and LMM was increased by 16 % and 18 % for participants in the highest quartile of UPF consumption (HR [95 % CI] (for LMS): 1.16 [1.05, 1.28], P = 0.012; HR [95 % CI] (for LMM): 1.18 [1.03, 1.35], P = 0.015). High berries intake may counteract the increased risk of LMS in participants with high UPF consumption (HR [95 % CI]: 1.10 [0.91, 1.34], P = 0.334). High dose of EBE alleviated the decrease of muscle strength (P = 0.036) and function caused by BD in rats. Furthermore, the co-incubation of EBE and AGEs improved L6 myoblasts proliferation (P = 0.033) and differentiation (P = 0.031). AGE-RAGE signaling pathway was predicted by network pharmacology and verified to be involved in the protective effects of EBE on muscle and L6 myoblasts against dietary AGEs toxicity. Besides, EBE can better ameliorate the AGEs-caused detriment of proliferation and differentiation in L6 myoblasts than single anthocyanin. Conclusions: These data supported the role for dietary AGEs in facilitating muscle damage, and suggested the importance of EBE consumption as a potential preventive strategy against dietary AGEs-induced muscle damage. |
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