FOOD AND CHEMICAL TOXICOLOGY
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2019
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IF 3.775
Wei Yang,Zhi-Kai Tian,Hui-Xin Yang,Zhao-Jun Feng,Jian-Mei Sun,Hong Jiang,Chao Cheng,Qing-Lei Ming,Chan-Min Liu
Fisetin , a natural flavonoid found in plants, fruits and vegetables, exerts anti-cancer, anti-oxidant, anti-inflammatory and anti-mitotic effects. The current study instigates the protective effect of fisetin against lead-induced synaptic dysfunction, neuroinflammation and neurodegeneration in mice, and explores its underlying mechanisms. The results indicated fisetin can significantly ameliorated behavioral impairments in Pb-treated mice. Fisetin inhibited Pb-induced the apoptotic neurodegeneration, as indicated by the decreased levels of Bax and cleaved caspase-3. Fisetin suppressed activations of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), NF-κB and subsequently inactivate pro-inflammatory factor including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). It can also decrease the accumulation of p-tau and amyloid-beta (Aβ) and increased the expression of the Aβ remover neprilysin (NEP) in brains of mice. Fisetin also reversed Pb-induced synaptic dysfunction by increasing the levels of synaptosomal associated protein-25 (SNAP-25), postsynaptic density-95 (PSD-95), cyclic-AMP-response element-binding protein (CREB) phosphorylation and calcium/calmodulin kinase II (CaMKII) phosphorylation. Fisetin promoted Pb-induced autophagy in the brains of mice. Moreover, fisetin can increase levels of the denosine 5′-monophosphate-activated protein kinase (AMPK) phosphorylation and SIRT1. Fisetin may be developed as a potential nutritional target for the prevention of Pb-induced neurotoxicity .
研究领域:
神经科学
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药理学
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毒理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food Bioscience
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2026
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IF 6.2
Qing Liu,Zengying Sui,Shiyi Li,Miaomiao Wan,Meilan Xue,Xia Qiu,Hui Liang,Lirui Sun
Fucoidan is a sulfated polysaccharide derived from brown algae ( Saccharina japonica ), and exhibits immunomodulatory properties. Emerging evidence suggests a strong correlation between the development of food allergy and intestinal dysfunction. The present study aimed to investigate the potential anti-food allergy activity of fucoidan and to elucidate its mechanism at the intestinal barrier function. The ovalbumin (OVA)-induced allergy mouse model was established, exhibiting increased OVA-specific IgE, histamine, Th2 inflammatory response, and intestinal damage. Oral administration of fucoidan markedly alleviated allergic symptoms by inhibiting mast cell activation and modulating intestinal immune responses. Furthermore, fucoidan significantly ameliorated intestinal immunological dysregulation, maintained barrier integrity, modulated gut microbiota composition, and enhanced short-chain fatty acid (SCFA) production. Mechanistically, the protective effects of fucoidan were closely associated with activation of the AMPK/SIRT1/FOXO1 pathway, which correlated with improved intestinal barrier function. Collectively, these results demonstrate that fucoidan may protect against food allergy by enhancing intestinal barrier function, highlighting the potential of natural biological substances in addressing food allergy.
✓ 已验证
DOI
高影响因子
Animal Nutrition
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2026
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IF 8.3
Anran Wang,Jie Xu,Haoyue Guo,Dongxu Luo,Zhen Zhang,Chao Ran,Shuyan Miao,Zhigang Zhou
Fish oil is an essential lipid source in aquafeed due to its high polyunsaturated fatty acid content. However, its susceptibility to oxidation can harm aquatic animal health and growth. This study investigated the effects of oxidized fish oil (OFO) diet on hepatopancreas health of Macrobrachium rosenbergii , and the mechanism by which Cetobacterium somerae protects against oxidative damage induced by OFO diet. A total of 240 juvenile prawns (3.36 ± 0.02 g) were randomly allocated to three dietary treatments with four replicates of 20 prawns each for 8 weeks: Control (control diet with fresh fish oil diet), OFO (OFO diet), and OFO + Cet (OFO diet supplemented with C. somerae at 1.52 × 10 7 CFU/g). Compared with the OFO group, C. somerae intervention significantly reduced the levels of lipid peroxidation-related markers, including malondialdehyde (MDA), 5-hydroperoxyeicosatetraenoic acid (5-HETE), leukotriene B4 (LTB4), prostaglandins (PGs), and thromboxanes (TXs), while increasing hepatopancreatic antioxidant indicators, including total antioxidant capacity (T-AOC), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GSH-Px) ( P < 0.05). Moreover, it also reversed the OFO diet-induced alterations in the relative mRNA expression levels of ferroptosis-related genes ( acsl4 , tfr1 , gpx4 , and slc7a11 ) ( P < 0.05), potentially via the adenosine monophosphate (AMP)-activated protein kinase (AMPK)-sirtuin1 (SIRT1)-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signaling pathway. Serum acetic acid, a C. somerae metabolite, exhibited the most pronounced alteration in the C. somerae -treated group ( P = 0.004). Furthermore, 160 juvenile prawns (2.62 ± 0.12 g) were randomly divided into two groups with four replicates of 20 prawns in each for 4 weeks: OFO diet, OFO + 0.15% sodium acetate (0.15% NaAc). Supplementation with 0.15% NaAc in the OFO diet also effectively decreased the peroxides (MDA, 5-HETE, LTB4, and TXs) and reversed the OFO diet-induced alterations in the relative mRNA expression levels of ferroptosis-related genes ( acsl4 , tfr1 , gpx4 , and slc7a11 ) compared with OFO group ( P < 0.05), suggesting a contributory role of acetate in the functionality of C. somerae . Meanwhile, the elevated AMP/adenosine triphosphate (ATP) ratio and upregulated relative mRNA expression levels of acss1/2 , ampk, sirt1 , and pgc-1α ( P < 0.05) indicated that C. somerae- derived acetate activates AMP production, thereby activating the AMPK-SIRT1-PGC-1α signaling pathway . Overall, C. somerae protects against OFO diet-induced hepatopancreatic injury by mitigating ferroptosis via acetate-mediated activation of the AMPK-SIRT1-PGC-1α signaling pathway.
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DOI
高影响因子
CHEMICAL ENGINEERING JOURNAL
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2024
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IF 13.3
Sijia Chen,Wanzhen Lei,Qi Liu,Xiaoting Wang,Kehan Chen,Xiaoyu Lin,Xuejiu Wang
Patients with diabetes frequently experience impaired wound healing, a challenge commonly attributed to immune imbalance and oxidative stress; notably, these issues arise from mitochondrial dysfunction. In this study, we fabricate a naturally derived bioactive hydrogel by incorporating resveratrol-loaded mesoporous polydopamine nanoparticles into silk microfibers-reinforced methacrylated silk network (SS/MPDA@RES), which exhibits appropriate injectability, light-curable performance and mechanical strength. It effectively scavenges excessive ROS to protect mitochondria, restore ATP production and remodel redox homeostasis. More importantly, it promotes mitochondrial biogenesis, respiratory capacity and oxidative phosphorylation via the AMPK/SIRT1/PGC-1α signaling axis, thereby reprogramming macrophages to the anti-inflammatory phenotype. In vivo , SS/MPDA@RES hydrogel promotes wound healing in diabetic rats by modulating immunity, inhibiting early inflammation, and accelerating angiogenesis and collagen deposition. Targeting mitochondria to regulate immune and redox homeostasis provides a novel avenue for the design of future tissue regeneration materials, with SS/MPDA@RES emerging as a potential treatment strategy for diabetic wounds.
研究领域:
材料科学
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生物材料
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组织工程
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免疫学
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糖尿病研究
✓ 已验证
产品关联
DOI
高影响因子
ACTA PHARMACOLOGICA SINICA
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2023
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IF 8.2
Xu Jia-wen,Xu Xu,Ling Yun,Wang Yan-chun,Huang Yu-jie,Yang Juan-zhen,Wang Jia-ying,Shen Xu
Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, which has yet no curable medication. Neuroinflammation and mitochondrial dysfunction are tightly linked to DPN pathology. G-protein-coupled receptor 40 (GPR40) is predominantly expressed in pancreatic β-cells, but also in spinal dorsal horn and dorsal root ganglion (DRG) neurons, regulating neuropathic pain. We previously have reported that vincamine (Vin), a monoterpenoid indole alkaloid extracted from Madagascar periwinkle , is a GPR40 agonist. In this study, we evaluated the therapeutic potential of Vin in ameliorating the DPN-like pathology in diabetic mice. Both STZ-induced type 1 (T1DM) and db/db type 2 diabetic (T2DM) mice were used to establish late-stage DPN model (DPN mice), which were administered Vin (30 mg·kg -1 ·d -1 , i.p.) for 4 weeks. We showed that Vin administration did not lower blood glucose levels, but significantly ameliorated neurological dysfunctions in DPN mice. Vin administration improved the blood flow velocities and blood perfusion areas of foot pads and sciatic nerve tissues in DPN mice. We demonstrated that Vin administration protected against sciatic nerve myelin sheath injury and ameliorated foot skin intraepidermal nerve fiber (IENF) density impairment in DPN mice. Moreover, Vin suppressed NLRP3 inflammasome activation through either β-Arrestin2 or β-Arrestin2/IκBα/NF-κB signaling, improved mitochondrial dysfunction through CaMKKβ/AMPK/SIRT1/PGC-1α signaling and alleviated oxidative stress through Nrf2 signaling in the sciatic nerve tissues of DPN mice and LPS/ATP-treated RSC96 cells. All the above-mentioned beneficial effects of Vin were abolished by GPR40-specific knockdown in dorsal root ganglia and sciatic nerve tissues. Together, these results support that pharmacological activation of GPR40 as a promising therapeutic strategy for DPN and highlight the potential of Vin in the treatment of this disease.
研究领域:
药理学
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神经科学
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内分泌学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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