Molecular biology reports · 2026
Ameliorative effect of MPAF on DSS-induced ulcerative colitis mice.
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Shan Chunlan, Liu Shunxing, Shi Xiaoli, Huang Yao, Miao Fujun
Аннотация
BACKGROUND: Ulcerative Colitis (UC) is a common chronic inflammatory intestinal disease. The nut protein peptides are not only easily digested and absorbed, but also possess various physiological functions. This study aims to investigate the protective effects of the Macadamia nut-derived peptide Ala-Cys-Asn-Pro-Phe-Gly-Trp (MPAF) against dextran sulfate sodium (DSS)-induced colitis in mice.
METHODS AND RESULTS: C57BL/6 mice were randomly divided into 5 groups (n = 10): the control group (CON), the DSS group, the low-dose MPAF group (MPAF-L, 50 mg/kg), the high-dose MPAF group (MPAF-H, 100 mg/kg), and 5-Aminosalicylic acid (5-ASA, 100 mg/kg) group. Colon, serum and liver tissues were collected to measure histopathology, antioxidant activity, and the expression levels of genes and proteins associated with the nuclear factor kappa B/NOD-like receptor protein 3 (NF-κB/NLRP3) pathway. Compared to the DSS group, the MPAF and 5-ASA groups exhibited alleviated colon atrophy (the colon length increased by 11.70% and DAI scores decreased by 20.73% in MPAF-H group), attenuated histopathological damage, significant increase in goblet cell numbers (P < 0.05 or P < 0.01), and upregulation of tight junction protein zonula occluden-1 (ZO-1) and mucoprotein-2 (MUC2) (P < 0.01). MPAF and 5-ASA also effectively enhanced antioxidant levels in UC colons (DSS vs. MPAF, P < 0.01), significantly inhibited the expression levels of key factors in the NF-κB/NLRP3 pathway, and reduced pro-inflammatory factors (DSS vs. MPAF-H, P < 0.01).
CONCLUSIONS: These findings indicate that MPAF could alleviate oxidative stress and inflammatory responses in the colon, protect the intestinal barrier, and mitigate pathological damage in UC mice. The underlying mechanism may involve suppression of the NF-κB/NLRP3 inflammatory pathway. These results support the potential of MPAF as a functional food ingredient for UC prevention and treatment.
METHODS AND RESULTS: C57BL/6 mice were randomly divided into 5 groups (n = 10): the control group (CON), the DSS group, the low-dose MPAF group (MPAF-L, 50 mg/kg), the high-dose MPAF group (MPAF-H, 100 mg/kg), and 5-Aminosalicylic acid (5-ASA, 100 mg/kg) group. Colon, serum and liver tissues were collected to measure histopathology, antioxidant activity, and the expression levels of genes and proteins associated with the nuclear factor kappa B/NOD-like receptor protein 3 (NF-κB/NLRP3) pathway. Compared to the DSS group, the MPAF and 5-ASA groups exhibited alleviated colon atrophy (the colon length increased by 11.70% and DAI scores decreased by 20.73% in MPAF-H group), attenuated histopathological damage, significant increase in goblet cell numbers (P < 0.05 or P < 0.01), and upregulation of tight junction protein zonula occluden-1 (ZO-1) and mucoprotein-2 (MUC2) (P < 0.01). MPAF and 5-ASA also effectively enhanced antioxidant levels in UC colons (DSS vs. MPAF, P < 0.01), significantly inhibited the expression levels of key factors in the NF-κB/NLRP3 pathway, and reduced pro-inflammatory factors (DSS vs. MPAF-H, P < 0.01).
CONCLUSIONS: These findings indicate that MPAF could alleviate oxidative stress and inflammatory responses in the colon, protect the intestinal barrier, and mitigate pathological damage in UC mice. The underlying mechanism may involve suppression of the NF-κB/NLRP3 inflammatory pathway. These results support the potential of MPAF as a functional food ingredient for UC prevention and treatment.