AQUACULTURE NUTRITION
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2026
·Vol. 2026
·期 1
·4395252
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IF 4.6
Haoran Yin,Lixing Wang,Zexin Lin,Ruilin Li,Qinxiao Cai,Zhiyu Zhou,Xiaoyi Wu
The hybrid grouper ( Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂), a typical carnivorous fish, has a limited ability to utilize dietary carbohydrates (CHOs). This study investigated the effects of different dietary arginine (Arg) levels (2.55 and 3.65%) and CHO-to-lipid ratios (C/L: 3.57, 2.39, 1.61) on the glycometabolism of hybrid grouper. Juvenile hybrid grouper (mean initial body length and weight: 7.8 cm and 13.04 g) were manually fed to fullness two times per day throughout a 7-week growth trial. The results showed that the C/L3.67 diets significantly elevated 2-h postprandial blood glucose concentration, as well as reduced hepatic glycogen level, intraperitoneal fat ratio (IPF), and the whole-body and hepatic lipid contents relative to the C/L2.39 and C/L1.61 diets. Dietary Arg supplementation significantly improved this metabolic disorder. These improvements were associated with enhanced plasma insulin-like growth factor 1 (IGF-1) concentration, hepatic phosphofructokinase (PFK) activity, nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) levels. They were also linked to the upregulated expression of key molecules in related pathways, including IGF-1 receptor (igf1r), phosphatidylinositol 3-kinase (pi3k), protein kinase AMP-activated catalytic subunit α (ampk-α), and protein kinase B (Akt) genes, as well as glucose transporter 4 (GLUT4) and mechanistic target of rapamycin (mTOR) proteins. Generally, suitable dietary Arg supplementation can reduce postprandial blood glucose and hepatic glycogen concentrations in hybrid grouper fed high C/L diets by regulating key genes and proteins within the IGF-1 and NO-cGMP pathways. This finding provided a nutritional intervention to enhance CHO utilization in hybrid grouper aquaculture.
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Biology-Basel
·
2025
·Vol. 14
·期 8
·992
·
IF 3.5
Kaicheng Gu,Lindong Yang,Yi Jiang,Zhiqiang Wang,Jiannan Chen
Simple SummaryBisphenol E (BPE), a typical endocrine disruptor, is widely present in various environmental media. Using zebrafish as a model, this study systematically evaluated the toxic effects of BPE on embryonic development and the nervous system. By integrating a network toxicology analysis and molecular docking techniques, the neurotoxic mechanism was revealed: BPE inhibits the activity of NOS3/PKG, blocks the transmission of the cGMP/PKG signaling pathway, and ultimately induces neurotoxic damage. This research advances the understanding of endocrine disruptor toxicity by providing novel experimental evidence and delivers key theoretical pillars for building a health risk assessment system targeting environmental pollutants.As typical environmental hormones, endocrine-disrupting chemicals (EDCs) have become a global environmental health issue of high concern due to their property of interfering with the endocrine systems of organisms. As a commonly used substitute for bisphenol A (BPA), bisphenol E (BPE) has been frequently detected in environmental matrices such as soil and water in recent years. Existing research has unveiled the developmental and reproductive toxicity of BPE; however, only one in vitro cellular experiment has preliminarily indicated potential neurotoxic risks, with its underlying mechanisms remaining largely unelucidated in the current literature. Potential toxic mechanisms and action targets of BPE were predicted using the zebrafish model via network toxicology and molecular docking, with RT-qPCRs being simultaneously applied to uncover neurotoxic effects and associated mechanisms of BPE. A significant decrease (p< 0.05) in the frequency of embryonic spontaneous movements was observed in zebrafish at exposure concentrations ≥ 0.01 mg/L. At 72 hpf and 144 hpf, the larval body length began to shorten significantly from 0.1 mg/L to 1 mg/L, respectively (p< 0.01), accompanied by a reduced neuronal fluorescence intensity and a shortened neural axon length (p< 0.01). By 144 hpf, the motor behavior in zebrafish larvae was inhibited. Through network toxicology and molecular docking, HSP90AB1 was identified as the core target, with the cGMP/PKG signaling pathway determined to be the primary route through which BPE induces neurotoxicity in zebrafish larvae. BPE induces neuronal apoptosis and disrupts neurodevelopment by inhibiting the cGMP/PKG signaling pathway, ultimately suppressing the larval motor behavior. To further validate the experimental outcomes, we measured the expression levels of genes associated with neurodevelopment (elavl3,mbp,gap43,syn2a), serotonergic synaptic signaling (5-ht1ar,5-ht2ar), the cGMP/PKG pathway (nos3), and apoptosis (caspase-3,caspase-9). These results offer crucial theoretical underpinnings for evaluating the ecological risks of BPE and developing environmental management plans, as well as crucial evidence for a thorough comprehension of the toxic effects and mechanisms of BPE on neurodevelopment in zebrafish larvae.
研究领域:
环境毒理学
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神经毒理学
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发育生物学
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分子生物学
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生态毒理学
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PubMed
高影响因子
JOURNAL OF MEDICINAL CHEMISTRY
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2024
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IF 6.8
Zheng-Jiong Zhao,Mei-Yan Jiang,Meng-Xing Huang,Yi-Yi Yang,Ling-Ling Feng,Chen Zhang,Yi-You Huang,Hai-Bin Luo,Yinuo Wu
Liver fibrosis is a common pathological feature of most chronic liver diseases with no effective drugs available. Phosphodiesterase 1 (PDE1), a subfamily of the PDE super enzyme, might work as a potent target for liver fibrosis by regulating the concentration of cAMP and cGMP. However, there are few PDE1 selective inhibitors, and none has been investigated for liver fibrosis treatment yet. Herein, compound AG-205/1186117 with the dihydropyrimidine scaffold was selected as the hit by virtual screening. A hit-to-lead structural modification led to a series of dihydropyrimidine derivatives. Lead 13h exhibited the IC50 of 10 nM against PDE1, high selectivity over other PDEs, as well as good safety properties. Administration of 13h exerted significant anti-liver fibrotic effects in bile duct ligation-induced fibrosis rats, which also prevented TGF-β-induced myofibroblast differentiation in vitro, confirming that PDE1 could work as a potential target for liver fibrosis.
研究领域:
药理学
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药物化学
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肝病学
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PubMed
高影响因子
AQUATIC TOXICOLOGY
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2025
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IF 4.3
Hao Chen,Guiqing Wu,Chunli Jiao,Lizhu Chen,Chunxiao Sun,Xinze Zhang,Xiao Wei,Xueping Wu,Dinglong Yang,Jianmin Zhao
Nitrite (NO 2 − ) and bifenthrin (BF), common environmental pollutant, have been proven to perform toxic effects on marine organisms. To have a better understanding of their effects on marine organism, Haliotis discus hannai was exposed to 0.1 mg/L NO 2 − and/or 10 μg/L BF for 28 days. The results showed that the gills in direct contact with the water environment exhibited the highest levels of BF bioaccumulation (89.37–142.36 μg/kg), especially after NO 2 − exposure ( P < 0.05). Transcriptome analysis of gills showed that significant enrichments were observed in metabolic, signaling and immune pathways after exposure, such as cGMP-PKG signaling pathway. Additionally, superoxide dismutase (SOD) activity was decreased in gills after exposure to NO 2 − and/or BF, parallel with the increase in catalase (CAT) activity, malondialdehyde (MDA) content, and total antioxidant capacity (AOC). Regarding genes related to immune, the expression of Defensin was significantly decreased while the expressions of B-cell lymphoma-2 ( Bcl-2 ), Tumor Necrosis Factor-α ( TNF-α ) and Caspase3 were increased. These results suggested that NO 2 − and BF exposure disrupted metabolic processes, impaired immune function, and dysregulated antioxidant defenses in the gills of abalone. Particularly, significant alterations were observed under the combined stress of NO 2 − and BF. In hemocytes, the ROS production could be induced by NO 2 − and/or BF stress, and the number of hemocytes and phagocytosis decreased significantly, especially in NO 2 − and BF groups. Integrated biomarker response (IBR) analysis proved that NO 2 − and/or BF exposure detrimentally affected the overall fitness of abalone, and combined NO 2 − and BF stress was the most stressful condition. This study emphasizes the impact of NO 2 − and/or BF on the abalone to better elucidate the risk of environmental pollution on abalone.
研究领域:
海洋毒理学
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环境科学
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水生生态学
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免疫学
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分子生物学
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高影响因子
BIOMEDICINE & PHARMACOTHERAPY
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2024
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IF 6.9
Yingying Jiang,Yu Cao,Yaoqi Li,Liuliu Bi,Lv Wang,Qianqian Chen,Yue Lin,Huanzhi Jin,Xiaoming Xu,Renyi Peng,Zheyan Chen
The incidence of diabetes is increasing annually, and the disease is uncurable due to its complex pathogenesis. Therefore, understanding diabetes pathogenesis and developing new treatments are crucial. This study showed that the NO donor SNP (8 µM) significantly alleviated high glucose-induced developmental toxicity in zebrafish larvae. High glucose levels caused hyperglycemia, leading to oxidative stress and mitochondrial damage from excessive ROS accumulation. This promoted mitochondrial-dependent apoptosis and lipid peroxidation (LPO)-induced ferroptosis, along with immune inflammatory reactions that decreased mitochondrial function and altered intracellular grid morphology, causing imbalanced kinetics and autophagy. After SNP treatment, zebrafish larvae showed improved developmental toxicity and glucose utilization, reduced ROS accumulation, and increased antioxidant activity. The NO-sGC-cGMP signaling pathway, inhibited by high glucose, was significantly activated by SNP, improving mitochondrial homeostasis, increasing mitochondrial count, and enhancing mitochondrial function. It's worth noting that apoptosis, ferroptosis and immune inflammation were effectively alleviated. In summary, SNP improved high glucose-induced developmental toxicity by activating the NO-sGC-cGMP signaling pathway to reduce toxic effects such as apoptosis, ferroptosis and inflammation resulting from mitochondrial homeostasis imbalance.
研究领域:
糖尿病
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发育生物学
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毒理学
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斑马鱼
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PubMed
高影响因子
Food Bioscience
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2025
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IF 5.9
Jialing Cao,Rong Tsao,Cheng Yang,Yun Wang,Lianfu Zhang
Red ginseng has been used to ameliorate erectile dysfunction (ED), a common age-related male reproductive disorder, though the active constituents responsible for this effect remain unclear. Arginyl-fructosyl-glucose (AFG) and arginyl-fructose (FA), are two arginine-derived Amadori compounds formed via Maillard reaction during red ginseng processing. An optimized vacuum dehydration method yielded 64.58% and 87.95%, respectively for AFG and FA, a significant increase compared to previous reported best results. In D-galactose-induced aging ED rats, the prepared AFG and FA significantly improved erectile function by reducing fibrosis and alleviating oxidative stress in the penile corpus cavernosum (PCC), alongside up-regulation of the eNOS/NO/cGMP signaling pathway within PCC. AFG and FA co-administration with 20(S)-ginsenoside Rg3 further enhanced the efficacy. These findings identify AFG and FA as key bioactives mediating the ED-improving effects of red ginseng and provide novel insights for red ginseng-based functional food development.
研究领域:
生药学
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天然产物化学
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衰老研究
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泌尿学
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功能食品
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高影响因子
Materials Today Bio
·
2024
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IF 8.7
Yannan Cheng,Yuanfang Huo,Yongle Yu,Ping duan,Xianzhen Dong,Zirui Yu,Qiang Cheng,Honglian Dai,Zhenyu Pan
Managing bone defects remains a formidable clinical hurdle, primarily attributed to the inadequate orchestration of vascular reconstruction and osteogenic differentiation in both spatial and temporal dimensions. This challenge persists due to the constrained availability of autogenous grafts and the limited regenerative capacity of allogeneic or synthetic bone substitutes, thus necessitating continual exploration and innovation in the realm of functional and bioactive bone graft materials. While synthetic scaffolds have emerged as promising carriers for bone grafts, their efficacy is curtailed by deficiencies in vascularization and osteoinductive potential. Nitric oxide (NO) plays a key role in revascularization and bone tissue regeneration, yet studies related to the use of NO for the treatment of bone defects remain scarce. Herein, we present a pioneering approach leveraging a photothermal-responsive system to augment NO release. This system comprises macromolecular mPEG-P nanoparticles encapsulating indocyanine green (ICG) (NO-NPs@ICG) and a mPEG-PA-PP injectable thermosensitive hydrogel carrier. By harnessing the synergistic photothermal effects of near-infrared radiation and ICG, the system achieves sustained NO release, thereby activating the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) signaling pathway both in vitro and in vivo. This orchestrated cascade culminates in the facilitation of angiogenesis and osteogenesis, thus expediting the reparative processes in bone defects. In a nutshell, the NO release-responsive system elucidated in this study presents a pioneering avenue for refining the bone tissue microenvironment and fostering enhanced bone regeneration.
研究领域:
生物材料
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组织工程
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再生医学
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生物医学工程
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药学
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高影响因子
Nature Communications
·
2024
·Vol. 15
·期 1
·1-18
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IF 14.7
Weng Haobo,Zou Weijuan,Tian Fangyan,Xie Huilin,Liu Ao,Liu Wen,Liu Yu,Zhou Nianwei,Cai Xiaojun,Wu Jianrong,Zheng Yuanyi,Shu Xianhong
Heart failure causes considerable morbidity and mortality worldwide. Clinically applied drugs for the treatment of heart failure are still severely limited by poor delivery efficiency to the heart and off-target consumption. Inspired by the high heart delivery efficiency of inhaled drugs, we present an inhalable cardiac-targeting peptide (CTP)-modified calcium phosphate (CaP) nanoparticle for the delivery of TP-10, a selective inhibitor of PDE10A. The CTP modification significantly promotes cardiomyocyte and fibroblast targeting during the pathological state of heart failure in male mice. TP-10 is subsequently released from TP-10@CaP-CTP and effectively attenuates cardiac remodelling and improved cardiac function. In view of these results, a low dosage (2.5 mg/kg/2 days) of inhaled medication exerted good therapeutic effects without causing severe lung injury after long-term treatment. In addition, the mechanism underlying the amelioration of heart failure is investigated, and the results reveal that the therapeutic effects of this system on cardiomyocytes and cardiac fibroblasts are mainly mediated through the cAMP/AMPK and cGMP/PKG signalling pathways. By demonstrating the targeting capacity of CTP and verifying the biosafety of inhalable CaP nanoparticles in the lung, this work provides a perspective for exploring myocardium-targeted therapy and presents a promising clinical strategy for the long-term management of heart failure.
研究领域:
心脏病学
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纳米医学
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药理学
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分子生物学
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高影响因子
BEHAVIOURAL BRAIN RESEARCH
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2023
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IF 2.7
Wenjie Chen,Yiping Chen,Muhammad Shahzad Aslam,Junliang Shen,Tao Tong,Simin Yan,Wenjing Cheng,Zichun Huang,Jiawei Li,Siyu Liu,Jianguo Li,Xianjun Meng
Background Depression is a severe emotional condition that significantly affects the quality of life. Acupuncture exerts preventive effects on depression in rats with post-chronic unpredictable mild stress (CUMS). Methods The study involved chronic unpredictable mild stress (CUMS) depression model mice to administer acupuncture as a preventative measure to investigate the mechanism of acupuncture's antidepressant and observe the effect of acupuncture on impact via the Lateral Habenula (LHb) and Gut-Liver-Brain Axis. The researcher investigated molecules correlating with a nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway and assessed inflammation in the LHb and liver. In addition, 16 S rDNA bioinformatics study revealed the quantity and variety of gut microbiota. Rats were randomly divided into five groups: control (CON), CUMS, CUMS + acupuncture (AP), CUMS + fluoxetine (FX) and CUMS + N(G) -nitro -L- arginine methyl ester (LNAME) group. Except for the CON group, other rats were exposed to CUMS condition for 28 days. Simultaneously, manual acupuncture (at Fengfu and Shangxing acupoints, once every other day) and fluoxetine gavage (2.1 mg/kg, 0.21 mg/mL, daily) were conducted to the groups of AP and FX, respectively, after stressors. Rats in LNAME group were treated with LNAME normal saline (10 mg/kg, 1 mg/mL, i.p.) solution. Behavioural tests and biological detection methods were conducted sequentially to evaluate depressionlike phenotype in rats. Results The results showed CUMS induced depression-like behaviours, hyper-activation of NO/cGMP signaling pathway, inflammation in serum, LHb and liver, and dysbiosis of the gut microbiota. These changes could be prevented and ameliorated by acupuncture to varying extents. Conclusion Acupuncture prevented and attenuated depression-like phenotype induced by CUMS, possibly via regulating the NO/cGMP signaling pathway and thus improving inflammation in serum, LHb and liver, and gut microbiota dysbiosis. In addition, these can be evidence of the existence of the gut-liver-brain axis.
研究领域:
神经科学
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精神病学
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中医
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微生物学
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药理学
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Engineering
·
2023
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IF 12.8
Shuang Yang,Yixiu Zhao,Xiaoling Cheng,Tingting Zhan,Jiaying Tian,Xue Liu,Chunyue Ma,Zhiqi Wang,Luying Jin,Qian Liu,Yanli Wang,Jian Huang,Jinhui Wang,Yan Zhang,Baofeng Yang
Myocardial ischemia is a serious threat to human health, and vascular dysfunction is its main cause. Buxu Tongyu Granule (BXTY) is an effective traditional Chinese medicine (TCM) for treating myocardial ischemia. However, the underlying mechanism of BXTY is still unclear. In this study, we demonstrate that BXTY ameliorates myocardial ischemia by activating the soluble guanylate cyclase (sGC)–3′,5′-cyclic guanosine monophosphate (cGMP)–protein kinase G (PKG) signaling pathway in vascular smooth muscle cells (VSMCs) to dilate the arteries. BXTY was given by gavage for ten consecutive days before establishing an animal model of acute myocardial ischemia in mice via the intraperitoneal injection of pituitrin. The results showed that BXTY alleviated the symptoms of myocardial ischemia induced by pituitrin in mice, including electrocardiogram abnormalities and changes in plasma enzymes. In addition, BXTY dilated pre-constricted blood vessels and inhibited the vasoconstriction of the superior mesenteric artery in a dose-dependent but endothelial-independent manner. These effects were eliminated by pre-incubating vascular rings with the sGC inhibitors NS 2028 or ODQ, or with the PKG inhibitor KT 5823. Moreover, BXTY increased the protein expression of sGC-β 1 and the intracellular second messenger cGMP level in mouse aortic vascular smooth muscle cells (MOVAs). NS 2028 or ODQ reversed these effects of BXTY. The expression level of the cGMP downstream effector protein PKG-1 increased after treating MOVAs with BXTY. NS 2028, ODQ, or KT 5823 also reversed this effect of BXTY. In conclusion, BXTY can improve the symptoms of acute myocardial ischemia in mice, and activating the sGC–cGMP–PKG pathway in VSMCs to induce vasodilation is its key pharmacodynamic mechanism.
研究领域:
药理学
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心脏病学
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中医药
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高影响因子
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
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2022
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IF 3.511
Wentao Sun,Yang Zhou,Hongmei Xue,Haitao Hou,Guowei He,Qin Yang
Although the association of elevated homocysteine level with cardiac hypertrophy has been reported, the molecular mechanisms by which homocysteine induces cardiac hypertrophy remain inadequately understood. In this study we aim to uncover the roles of cyclic nucleotide phosphodiesterase 1 (PDE1) and endoplasmic reticulum (ER) stress and their relationship to advance the mechanistic understanding of homocysteine-induced cardiac cell hypertrophy. H9c2 cells and primary neonatal rat cardiomyocytes are exposed to homocysteine with or without ER stress inhibitor TUDCA or PDE1-specific inhibitor Lu AF58027, or transfected with siRNAs targeting PDE1 isoforms prior to homocysteine-exposure. Cell surface area is measured and ultrastructure is examined by transmission electron microscopy. Hypertrophic markers, PDE1 isoforms, and ER stress molecules are detected by q-PCR and western blot analysis. Intracellular cGMP and cAMP are measured by ELISA. The results show that homocysteine causes the enlargement of H9c2 cells, increases the expressions of hypertrophic markers β-MHC and ANP, upregulates PDE1A and PDE1C, promotes the expressions of ER stress molecules, and causes ER dilatation and degranulation. TUDCA and Lu AF58027 downregulate β-MHC and ANP, and alleviate cell enlargement. TUDCA decreases PDE1A and PDE1C levels. Silencing of PDE1C inhibits homocysteine-induced hypertrophy, whereas PDE1A knockdown has minor effect. Both cAMP and cGMP are decreased after homocysteine-exposure, while only cAMP is restored by Lu AF58027 and TUDCA. TUDCA and Lu AF58027 also inhibit cell enlargement, downregulate ANP, β-MHC and PDE1C, and enhance cAMP level in homocysteine-exposed primary cardiomyocytes. ER stress mediates homocysteine-induced hypertrophy of cardiac cells via upregulating PDE1C expression Cyclic nucleotide, especially cAMP, is the downstream mediator of the ER stress-PDE1C signaling axis in homocysteine-induced cell hypertrophy.
研究领域:
心脏病学
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分子生物学
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细胞生物学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Linlin Liu,Mozhu Jin,Xueying Han,Deqiang Dou
Ethnopharmacological relevance The nature of Chinese medicine is a unique index to measure its efficacy. Generally, treating the hot syndrome with cold nature medicine and vice versa. Ginseng medicines, a renowned Chinese medicine known for its qi tonifying action, encompasses various herbal materials such as ginseng, red ginseng, and black ginseng (GS, RG, and BG, respectively), ginseng leaves (GL), and American ginseng (AG), which exhibited different natures, thought contained similar ginsenosides. This traditional effect of GS and RG “reinvigorate the pulse for relieving qi depletion”. It is closely linked to anti-heart failure (HF), HF is a clinical manifestation of deficiency of “heart- qi ”. However, the elucidation of the mechanism underlying the anti-HF effects of ginseng medicines with different natures remains a significant challenge. Aim of the study To elucidate pharmacological mechanisms underlying the effect of ginseng medicines on HF, and to identify biomarkers associated with their various natures. Furthermore, it provides the basis for the different applications of ginseng medicines with various natures. Materials and methods This study established a rat model of HF induced by isoproterenol (ISO) combined with a specific diet. Four representative hot / cold herbs were selected as compared references for the medicine natures. The divergent effects of these herbs on the HF model were investigated by analyzing RNA-seq data to identify genes expressed differentially. Additionally, pathways associated with medicine natures were obtained using KEGG. Furthermore, UPLC-QqQ-MS/MS, as well as ELISA, were used to measure indexes associated with the nervous system, energy metabolisms, and endocrinology systems, such as BNP, CK, IL-1, T3, T4, cAMP, cGMP, AD, adrenal hormones (DOC, CORT, and COR), progestogens (pregnenolone, P, 17-OH-PR, and 17-OH-P), androgens (DHEA, A4, and T), and estrogens hormones (E2). Results All ginseng medicines demonstrated varying levels of efficacy in alleviating HF and GS exhibited a significant protective effect on HF. The ginseng medicines with qi tonifying primarily achieve their effect by enhancing the levels of adrenal hormones (DOC, CORT, and COR), T4, elevation of cAMP/cGMP, and activation of AchE. Warm nature qi tonifying ginseng medicines increased the levels of 17-OH-PR and P while decreasing 17-OH-P and the ratio of E2/T. On the other hand, cold nature qi tonifying ginseng medicines decreased the levels of A4 and T while increasing the ratio of E2/T. Conclusion Overall, the effects of warm nature ginseng medicines are stronger on HF compared to cold nature ginseng medicines. Our research firstly reported that the E2/T ratio, progestogens (17-OH-PR, 17-OH-P, and P), and androgens (A4 and T) have been identified as significant biomarkers for discerning the mechanism differences of ginseng medicines with differences natures in treatment of HF.
研究领域:
民族药理学
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药理学
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分子生物学
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内分泌学
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心脏病学
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高影响因子
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