COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
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2020
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IF 2.897
Qing Zhang,Li-Chong Hao,Yu Hong
Diisononyl phthalate (DINP) as a phthalate plasticizer is widely used in daily life and production, which shows endocrine disruption effects and has several adverse effects on the normal physiological function. Here, the effects of DINP (0.1%, 0.2%, 0.5%, and 1.0%) (v/v) on the fertility, lifespan, climbing behavior, anti-starvation ability of Drosophila melanogaster and the potential modes of action were investigated. The results showed that DINP impaired fertility in a dose-dependent manner and smaller ovarian volume, lower hatching rate, and fewer offspring was observed at higher concentrations. The effect of DINP on the lifespan showed gender-specific, and mortality was increased after exposure above 0.2% DINP. The climbing ability increased at 0.1% DINP compared with the vehicle group, while it manifested a dose-dependent decrease at higher concentrations. The anti-starvation ability exhibited hormesis after short-term culture and reduced as culture time extending. By measuring the redox status (catalase (CAT) and reactive oxygen species (ROS)) of adult flies after two exposure methods, it was found that DINP induced redox instability, which may explain the above effects at the molecular level. This study provides data to support a comprehensive analysis of DINP potential toxicity and to guide its rational use and management better.
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Food Science and Human Wellness
·
2024
·
IF 5.6
Xiaomei Du,Kexin Wang,Xiaoyan Sang,Xiangxing Meng,Jiao Xie,Tianxin Wang,Xiaozhi Liu,Qun Huang,Nan Zhang,Hao Wang
Naringin exists in a wide range of Chinese herbal medicine and has proven to possess several pharmacological properties. In this study, PC12, HepG2 cells, and female Drosophila melanogaster were used to investigate the antioxidative and anti-aging effects of naringin and explore the underlying mechanisms. The results showed that naringin inhibited H 2 O 2 -induced decline in cell viability and decreased the content of reactive oxygen species in cells. Meanwhile, naringin prolonged the lifespan of flies, enhanced the abilities of climbing and the resistance to stress, improved the activities of antioxidant enzymes, and decreased malondialdehyde content. Naringin also improved intestinal barrier dysfunction and reduced abnormal proliferation of intestinal stem cells. Moreover, naringin down-regulated the mRNA expressions of inr , chico , pi3k , and akt-1 , and up-regulated the mRNA expressions of dilp2 , dilp3 , dilp5 , and foxo , thereby activating autophagy-related genes and increasing the number of lysosomes. Furthermore, the mutant stocks assays and computer molecular simulation results further indicated that naringin delayed aging by inhibiting the insulin signaling (IIS) pathway and activating the autophagy pathway, which was consistent with the result of network pharmacological predictions.
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INDUSTRIAL CROPS AND PRODUCTS
·
2026
·
IF 6.4
Lijuan Hou,Cheng Zhang,Ying Li,Wanchao Hou,Honggang Tang,Xing Zhang,Zhenyu Wang,Xianjun Dai
LBL-assembled MPN-LYS-PEC nanoparticles enable microbiota-targeted quercetin delivery. • The nanoparticles show high quercetin encapsulation and structural stability. • The nanoparticles alleviate HFD-induced intestinal injury in D. melanogaster . • Germ-free assays confirm a gut microbiota-dependent protective mechanism. Quercetin is a bioactive flavonoid; however, its poor stability and low bioavailability limit its protective effect against intestinal injury. To address this limitation, quercetin-Fe 2 + metal-phenolic network (MPN) nanocores are constructed using a solvent exchange method, followed by layer-by-layer electrostatic assembly with positively charged lysozyme (LYS) and negatively charged pectin (PEC) to form ternary MPN-LYS-PEC nanoparticles. Comprehensive physicochemical characterization confirms effective charge regulation and structural stability throughout the assembly process, together with a high quercetin encapsulation efficiency (92.57 ± 0.67%) and loading efficiency (25.98 ± 2.59%). The multilayered architecture further protects quercetin during gastrointestinal digestion, enabling microbiota-targeted delivery. In a high-fat diet (HFD)-induced female and male Drosophila melanogaster ( D. melanogaster ), the nanoparticles effectively reduced intestinal leakage, cell death, and oxidative stress, and improved metabolic dysregulation. They also beneficially reshaped gut microbiota by enriching Commensalibacter and reducing Novosphingobium . Importantly, experiments in germ‑free D. melanogaster further demonstrate that the gut‑protective effects induced by MPN‑LYS‑PEC nanoparticles are associated with the gut microbiota. Collectively, these findings establish the self-assembled MPN-LYS-PEC nanoparticle as an effective strategy for gut microbiota-targeted quercetin delivery, thereby alleviating HFD-induced intestinal injury and restoring metabolic homeostasis. Download: Download high-res image (184KB) Download: Download full-size image
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Food Bioscience
·
2026
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IF 6.2
Fenyi Min,Jiaqing Wang,Liping Qin,Yuxin Wang,Yizhou Li,Xuebo Liu,Lijun Sun
Plant-derived bioactive peptides have been suggested as a class of compounds with neuroprotective properties. This study focused on the cognitive-enhancing effects of Cyperus esculentus peptide (CEP) based on ‘in silico-drosophila-mice’ stepwise cognitive impairment models, followed by systematical elucidation in multi-target mechanism of its function. Specifically, network pharmacology prediction indicated that CEP exerted the modifying effects through essential nodes including cAMP signaling pathways and neuroinflammation regulation. Behavioral experiments confirmed that CEP effectively enhanced learning and memory capability of stress-modeled fruit flies and scopolamine-induced cognitive impairment mice. Then, mechanism investigation indicated that CEP could activate the cAMP-PKA-CREB-BDNF signaling axis within the central nervous system, enhancing synaptic plasticity (upregulated PSD-95 expression) while concurrently alleviating oxidative stress, cholinergic imbalance, and neuroinflammation. Additionally, CEP remodeled gut microbiota ecology, increasing beneficial bacteria abundance such as Akkermansia and Bifidobacterium and substantially enhancing short-chain fatty acid (SCFA) production. This further activated FFAR2/3 receptor signaling, restored intestinal barrier integrity and suppressed peripheral inflammation, indicating a neuroprotective pathway via the microbiota-gut-brain axis. Conclusively, this study confirmed CEP as a highly promising cognitive enhancer in a synergistic mode of coordinated regulation of central nervous and peripheral pathways, which provided theoretical underpinnings for intervention strategies of bioactive peptides in Cyperus esculentus targeting neurodegenerative diseases via the gut-brain axis.
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BIOORGANIC CHEMISTRY
·
2026
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IF 5.1
Qian Zhang,Wenyu Wang,Chenhan Wu,Qingting Du,Weili Yin,Jiaheng Chen,Jian Ma,Chong Li,Shaojie Zhang
Ulcerative colitis (UC) is characterized by recurrent inflammation of the gastrointestinal tract, and currently available treatment drugs are limited. Plant-derived polysaccharides hold promise for UC prevention. A water-soluble α -D-glucan (CLP80–1) with a molecular weight of 8.17 × 10 5 Da was isolated and characterized from the roots of traditional Chinese medicinal plant Crepis lignea . Structural analysis revealed that its repeating units comprise →6)- α -D-Glc p -(1 → and →3,6)- α -D-Glc p- (1 → residues as the backbone, with α -D-Glc p -(1 → as side chains substituted at C-3. The protective effects of CLP80–1 on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in Drosophila melanogaster were investigated. Our results demonstrated that treatment with 1% CLP80–1 significantly improved survival rates, attenuated gut atrophy, reduced intestinal permeability, enhanced intestinal barrier function, suppressed excessive proliferation of intestinal stem cells (ISCs) and enteroblasts (EBs), and inhibited the death of intestinal epithelial cells (IECs). Metabolomic and transcriptomic analyses revealed that CLP80–1 mainly affected amino acid metabolism, TCA cycle, oxidative phosphorylation and JAK/STAT signaling pathway. Furthermore, CLP80–1 reduced reactive oxygen species (ROS) levels, suppressed the expression of pro-inflammatory factors, and downregulated the JAK-STAT signaling pathway, thereby mitigating oxidative stress and inflammatory responses. These findings suggest that CLP80–1 is effective in alleviating intestinal inflammation and may serve as a promising therapeutic candidate for addressing gut inflammatory conditions.
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CELLULAR AND MOLECULAR LIFE SCIENCES
·
2026
·Vol. 83
·期 1
·219
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IF 6.5
Fan Xinxin,Yan Jinhua,Yuan Yu,Chen Yi,Chen Haiyang
The global incidence of inflammatory bowel disease (IBD) is rising, an epidemiological trend strongly linked to the increasing consumption of ultra-processed foods. Although certain food additives are implicated in IBD pathogenesis, the direct impact of these additives on intestinal stem cells (ISCs), key effectors of epithelial homeostasis and repair, is poorly defined. Specifically, 4-hexylresorcinol (4-HR), a widely used phenolic preservative, has not been thoroughly investigated for its long-term impact on intestinal health, particularly during inflammation and repair. Using a Drosophila melanogaster model of bleomycin (BLM)-induced intestinal injury, we combined genetic analysis, immunofluorescence staining, and functional assays to evaluate the effects of 4-HR on tissue pathology, ISC proliferation, and evolutionarily conserved pro-repair signaling pathways. Our findings indicate that 4-HR significantly aggravates intestinal damage and impedes epithelial regeneration by suppressing the injury-induced proliferation of ISCs. Mechanistic studies revealed that 4-HR inhibits the activation of the MAPK signaling pathway, which is critical for initiating the reparative program following injury. Importantly, we extend these findings to a mammalian system, demonstrating that 4-HR similarly impairs intestinal repair and suppresses the conserved MAPK signaling axis in a mouse model of colitis. Collectively, our data elucidate a previously unrecognized mechanism whereby the food additive 4-HR aggravates intestinal damage and impedes epithelial regeneration by directly suppression MAPK-dependent, ISC-driven repair. This cross-species validation establishes the detrimental role of 4-HR and its core mechanism as conserved from invertebrates to mammals, not only establishing a novel link between dietary factors and epithelial repair dysregulation but also underscoring a significant dietary environmental contributor to IBD pathogenesis. Furthermore, this study establishes a foundation for future research into how dietary components influence stem-cell biology, underscoring the urgent need to re-evaluate the long-term safety of common food additives in vulnerable populations.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
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IF 8.7
Su Jinle,Ge Lingrui,Niu Chunyu,Chen Yan,Zhang Leifang,Chen Yin
SP0–1, a neutral polysaccharide fraction isolated from sea buckthorn berries ( Hippophae rhamnoides L.), was purified and structurally characterized, and its antioxidant-related intestinal protective effects were evaluated in Drosophila melanogaster . HPGPC analysis showed a single symmetrical peak and indicated a relatively homogeneous fraction with a moderate molecular weight (Mw, 5.59 × 10 4 Da; ≈55.9 kDa). PMP-HPLC analysis revealed that SP0–1 was mainly composed of galactose, xylose, and arabinose (Gal/Xyl/Ara-rich; Gal:Xyl:Ara = 1:0.38:0.93). Methylation analysis combined with 1D/2D NMR spectroscopy supported the presence of major →4)- and →4,6)-linked Galp motifs, →5)- and →3,5)-linked Araf motifs, and terminal Xylp residues. The consecutive Gal–Gal arrangement, the residue adjacent to Gal O-6, the overall connection of the Ara/Xyl-containing region to the Gal-containing region, and the O-3 substituent of residue D remain unresolved. Functionally, SP0–1 exhibited concentration-dependent radical-scavenging activities against DPPH, ABTS• + , and hydroxyl radicals in vitro. In a Drosophila oxidative-stress model, dietary SP0–1 supplementation significantly improved survival and climbing performance, enhanced endogenous antioxidant enzyme activities, and reduced malondialdehyde levels. Moreover, SP0–1 markedly alleviated H 2 O 2 -induced intestinal oxidative injury, as evidenced by decreased reactive oxygen species accumulation and reduced intestinal epithelial cell death. These findings suggest that the structural characteristics of SP0–1, including its proposed Gal-rich linkage features and Ara/Xyl-containing residue motifs, may be associated with the observed antioxidant-related intestinal protection. Collectively, this study provides a structural and functional basis for further investigation of SP0–1 as a potential bioactive polysaccharide fraction.
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BRAIN RESEARCH BULLETIN
·
2018
·
IF 3.44
Tianhang Wang,Jiling Cheng,Shuyu Wang,Xudong Wang,Hongquan Jiang,Yueqing Yang,Ying Wang,Chunting Zhang,Weiwei Liang,Honglin Feng
Amyotrophic lateral sclerosis (ALS) is a degenerative disease with a progressive loss of motor neurons in the central nervous system (CNS). However, there are unsolved problems with the therapies for this disease. α-Lipoic acid (LA) is a natural, universal antioxidant capable of scavenging hydroxyl radicals as well as regenerating a series of antioxidant enzymes that has been widely used in clinical settings. This study aimed to evaluate the antioxidant and neuroprotective effects of LA in ALS cell and Drosophila models with mutant G85R and G93A hSOD1 genes. The biological effects of LA and the protein levels of several antioxidant factors were examined, as were those of phospho-Akt and phospho-ERK. Furthermore, specific inhibitors of the PI3K/Akt and MEK/ERK signaling pathways were used to analyze their effects on LA-induced antioxidant expression in vivo and in vitro . Evidences showed that the mutant hSOD1 resulted in the increased oxidative stress, abnormal antioxidant signaling and pathological behaviors in motor performance and survival compared with non-mutant hSOD1 models, treatment with LA improved motor activity and survival in transgenic flies, prevented NSC34 cells from mutant hSOD1 or H 2 O 2 induced decreased antioxidant enzymes as well as increased ROS levels. In addition, LA regulated the expression levels of antioxidant proteins in a dose- and periodical time-dependent manner, which might be mediated by ERK/Akt pathway activation and independent from the mutant hSOD1 gene. Our observations suggest that LA exerts strong and positive antioxidant and neuroprotective effects through the activation of the ERK-Akt pathway in hSOD1 ALS models.
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