PLoS One
·
2019
·Vol. 14
·期 5
·e0216711
·
IF 2.776
Xinyu Lin,Dingping Bai,Zixi Wei,Ying Zhang,Yifan Huang,Hui Deng,Xiaohong Huang
Large-scale breeding environments often lead to oxidative stress. Macrophages play an important role in the immune system and are vulnerable to reactive oxygen species (ROS), which result in macrophage death. Curcumin is the main active component of turmeric and exerts antioxidant effects. Here, we measured the activity of some antioxidant enzymes and chose the Nrf2-Keap1 signaling pathway to study the protective effects of curcumin on macrophages under oxidative stress in vitro. We used RAW264.7 cells as a research model, and oxidative damage was induced by hydrogen peroxide (H 2 O 2 ). Cell viability was measured by an MTT assay. Flow cytometry was used to measure cellular ROS and apoptosis. The effect of curcumin on Nrf2-Keap1 signaling pathway-related genes was analyzed by qRT-PCR. Furthermore, the translocation of Nrf2 protein was also investigated by Western blot analysis of total and nuclear proteins. All curcumin-treated groups exhibited increased activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). Low- and middle-dose curcumin decreased malondialdehyde (MDA) and ROS levels, but high-dose curcumin increased MDA and ROS production. We found that low-dose curcumin protected cells from apoptosis, while apoptosis in the middle- and high-dose curcumin-treated groups were stagnant in the early stage. Furthermore, middle-dose curcumin upregulated Nrf2 expression after H 2 O 2 treatment for 4 h. Low- and middle-dose curcumin could activate Nrf2 and promote it to migrate into nuclei. The translocation of Nrf2 to the nucleus to upregulate the expression of haemoxygenase-1 (HO-1) was promoted in the low- and middle-dose curcumin-treated groups. The middle-dose curcumin-treated group also exhibited enhanced expression of glutamate-cysteine ligase, a modifier subunit (GLCM), but inhibited transcription of glutamate-cysteine ligase, a catalytic subunit (GCLC). Curcumin resisted oxidants by increasing the activity of antioxidant enzymes and activating the Nrf2-Keap1 pathway, which could potentially promote cell survival.
研究领域:
免疫学
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药理学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
Frontiers in Nutrition
·
2022
·
IF 6.59
Chen Hui,Zheng Huizhen,Li Tiejun,Jiang Qihong,Liu Shulai,Zhou Xuxia,Ding Yuting,Xiang Xingwei
Oyster peptide (OP) has exhibited useful biological activities and can be used in multi-functional foods. OP has been reported to play a significant role in intestinal protection, but its specific mechanism is still not completely understood. The aim of this study was to analyze the potential effect of OP on oxidative damage of mice intestine induced by cyclophosphamide (Cy). The experimental results revealed that intragastric administration of OP significantly increased average bodyweight, improved ileum tissue morphology and villus structure, as well as increased the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in oxidized mice serum and liver. The content of malondialdehyde (MDA) in the mice serum and liver homogenate was found to be markedly decreased. Moreover, OP significantly increased the relative mRNA expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), quinone oxidoreductase (NQO1) and heme oxidase-1 (HO-1) in ileum. Western-blot results indicated that prior administration of OP significantly up-regulated the Nrf2 production in ileum, and substantially decreased then Keap1 gene expression. In conclusion, intake of OP was found to markedly improve intestinal oxidative stress in vivo, and this effect was primarily mediated through the simulation of antioxidant Nrf2-Keap1 signaling pathway. This study is beneficial to the application of peptide nutrients in the prevention or mitigation of intestinal oxidative damage.
研究领域:
营养学
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药理学
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分子生物学
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免疫学
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DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Xingyu Chen,Wenqian Sun,Yanting Song,Shangong Wu,Shouqi Xie,Wen Xiong,Chengdong Peng,Yu Peng,Zhengxiang Wang,Sovan Lek,Christer Hogstrand,Mette Sørensen,Lei Pan,Dong Liu
The impact of cadmium (Cd) toxicity on fish liver injury has received much attention in recent years. Currently, autophagy, apoptosis and endoplasmic reticulum stress were reported in Cd exposed fish liver, and if there are other mechanisms (such as ferroptosis) and relevant signaling pathways involved in fish remains unknown. An experiment was conducted to investigate Cd toxicity in Channa argus (Cantor, 1842) exposed to 0, 1.0, and 2.0 mg Cd/L of water for 96 h. Cd disrupted the structure of mitochondria in the liver. Besides, Cd induced ferroptosis by significantly increasing the level of Fe 2+ , ROS, MDA and significantly decreasing the level of Ferritin, GSH, GSH-Px, GPX4, GST and SOD ( p < 0.05 in all cases). In addition, the mRNA expression of ferroptosis related genes, gpx4 and slc7a11 , were significantly downregulated by Cd. Moreover, Cd exposure significantly inhibited the Nrf2/Keap1 signaling pathway, one of the pathways involved in ferroptosis, by upregulating the mRNA levels of keap1a and keap1b , and downregulating the mRNA levels of nrf2 and its target genes ( ho-1 , nqo1 and cat ). Cd exposure also caused extensive accumulation of vacuoles and lipid droplets in liver, as well as an increase in triglyceride content. Cd significantly affected lipid metabolism related enzyme activity and gene expression, which were also regulated by Nrf2/Keap1 signaling pathway. In summary, these results indicate that ferroptosis is a mechanism in waterborne Cd exposed fish liver injury via the Nrf2/Keap1 signaling pathway and the Cd induced hepatic steatosis is also modulated by Nrf2/Keap1 pathway at the whole-body level in fish. These findings provide new insights into the fish liver injury and molecular basis of Cd toxicity.
研究领域:
环境毒理学
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鱼类生理学
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分子生物学
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DOI
PubMed
高影响因子
Pharmaceuticals
·
2025
·Vol. 18
·期 4
·548
·
IF 4.8
Huiming Xue,Zhen Feng,Chang Jin,Yue Zhang,Yongxing Ai,Jing Wang,Meizhu Zheng,Dongfang Shi
Objectives: Ischemic stroke is a severe neurological disorder with high morbidity, mortality, and disability rates, posing a substantial burden on patients, families, and healthcare systems. Soy isoflavone (SI), a naturally occurring phytoestrogen, has demonstrated promising neuroprotective effects. This study aimed to evaluate the anti-stroke efficacy of SI and elucidate its underlying mechanisms through integrated phytochemical profiling, network pharmacology, and both in vitro and in vivo experimental validation.Methods: Active constituents of SI were extracted via reflux and identified using liquid chromatography–mass spectrometry (LC-MS). Network pharmacology was employed to predict therapeutic targets and signaling pathways. The neuroprotective effects of SI were first assessed in PC12 cells subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) injury in vitro. For in vivo evaluation, transient cerebral ischemia–reperfusion injury was induced using the bilateral common carotid artery occlusion (BCCAO) model in adult male ICR rats (27.3 ± 1.8 g; 6–8 weeks old), obtained from the Shanghai Experimental Animal Center, Chinese Academy of Sciences. Forty-eight rats were randomly assigned into four groups (n= 12): sham, model (BCCAO), SI-treated (100 mg/kg, oral gavage for 5 days), and edaravone (EDA)-treated (10 mg/kg, i.p., positive control). All procedures were approved by the Institutional Animal Care and Use Committee of Changchun Normal University (Approval No. 2024003, 13 March 2024) and conducted in accordance with the NIH guidelines and ARRIVE 2.0 reporting standards.Results: In vitro, SI significantly enhanced PC12 cell viability from 57.23 ± 2.88% to 80.76 ± 4.43% following OGD/R. It also reduced intracellular Ca2+by 58.42%, lactate dehydrogenase (LDH) release by 37.67%, caspase-3 activity by 55.05%, and reactive oxygen species (ROS) levels by 74.13% (p< 0.05). A flow cytometry analysis revealed that OGD/R increased the apoptosis rate from 5.34% (control) to 30.85% (model group), which was significantly attenuated by SI treatment, especially in the 560 µg/mL group (20.00%), followed by the 140 and 280 µg/mL groups. In vivo, SI improved neurological scores from 8.3 ± 1.09 to 6.8 ± 1.68, reduced cerebral infarction volume by 18.49%, and alleviated brain edema by 10.42% (p< 0.05). SI also decreased malondialdehyde (MDA) and LDH levels by 31.15% and 39.46%, respectively, while increasing the activity of antioxidant enzymes: superoxide dismutase (SOD) by 11.70%, catalase (CAT) by 26.09%, and glutathione peroxidase (GSH-px) by 27.55% (p< 0.01). Scratch assay results showed that SI restored the impaired migratory ability of the OGD/R-treated PC12 cells, further supporting its role in cellular repair. A Western blot analysis demonstrated the upregulation of nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1) and the downregulation of Kelch-like, ECH-associated protein 1 (Keap1) in the cerebral ischemia–reperfusion model.Conclusions: These findings indicate that soy isoflavone confers significant neuroprotective effects against cerebral ischemia–reperfusion injury by enhancing endogenous antioxidant defense mechanisms, reducing oxidative stress, inhibiting apoptosis, and promoting cell migration. The protective effects are likely mediated through the activation of the Nrf2/Keap1 signaling pathway, supporting the therapeutic potential of SI in ischemic stroke treatment.
研究领域:
药理学
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神经科学
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分子生物学
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PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2024
·
IF 7
Xinya Qi,Lingling Tong,Hui Lian,Zilei Chen,Linhui Yang,Yang Wu,Suxing Jin,Dongsheng Guo
Here, a high molecular weight polysaccharide preparation from Ophiocordyceps gracilis was utilized as a stabilizer and dispersant to create nanocomposites based on selenium nanoparticles (GSP-1a-SeNPs). The NPs showed the highest stability at a selenium/polysaccharide mass ratio of 1:1, with no significant change after 28 days of storage at 4 ℃. The NPs exhibited a symmetrical spheroid structure with an average diameter of 85.4 nm. Next, the anti-inflammatory properties and mechanisms of the GSP-1a-SeNPs were examined in LPS-induced RAW264.7 cells, which efficiently internalized the NPs. In the anti-inflammatory assays, GSP-1a-SeNPs significantly reduced the production of pro-inflammatory cytokines, including TNF-α and IL-6, and lowered ROS levels by activating the Nrf2-Keap1 pathway. This pathway regulates selenoprotein expression, thereby balancing the immune microenvironment of RAW264.7 cells and mitigating inflammation. These results suggest that GSP-1a-SeNPs could serve as potential therapeutic agents or adjuvants for treating LPS-induced inflammation.
研究领域:
药理学
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纳米医学
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免疫学
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产品关联
DOI
PubMed
高影响因子
Food & Function
·
2025
·
IF 5.4
Jiaxuan Li,Yu Li,Xunyu Song,Yuxiao Wang,Yinxu Zhang,Xinghua Gao,Mingqian Tan,Wentao Su
High-fat diets (HFDs) impair the intestinal barrier by increasing permeability and oxidative stress, which contributes to obesity-related disorders. Ulva lactuca, a marine green alga, produces extracellular vesicles (UEVs) that remain underexplored as functional food components. In this study, UEVs were isolated and characterized, showing a cup-like shape morphology with average diameter of 188.8 nm. Functional assays demonstrated that UEV treatment attenuated oxidative stress, reduced apoptosis, and restored tight junction proteins. In a gut-on-a-chip model, UEVs improved transepithelial electrical resistance (TEER) and enhanced mucin secretion under HFD-mimicking stress. Mechanistic studies revealed that UEVs activated the Nrf2/Keap1/HO-1 signaling pathway, promoting nuclear translocation of Nrf2 and upregulation of antioxidant genes. Collectively, these findings highlight UEVs as novel food-derived nanostructures with dual functions in oxidative stress reduction and intestinal barrier protection, supporting their potential in functional food applications targeting metabolic gut disorders.
研究领域:
海洋生物学
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营养科学
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分子生物学
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纳米技术
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胃肠病学
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产品关联
DOI
PubMed
高影响因子
HISTOLOGY AND HISTOPATHOLOGY
·
2026
·Vol. 41
·期 3
·453-465
·
IF 2.2
Xuefei Fan,Suhuan Chen,Haomiao Liu,Nannan Liu,Mengyan Zhang,Mengmeng Chen,Wuqi Chen,Guangyi Chen,Weilu Gao,Tao Yao,Xiaoyu Chen
Background: Rheumatoid arthritis can affect extra-articular organs such as the liver, and the problem of drug-induced liver injury caused by traditional antirheumatic drugs for improving the condition cannot be ignored. This study aims to investigate the therapeutic effects of resveratrol (Res) on hepatic inflammation and oxidative stress in mice with collagen-induced arthritis (CIA) and to elucidate the relationship between the regulatory mechanisms of the nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway. Methods: In this study, we used chicken type II collagen in combination with complete Freund's adjuvant to induce arthritis in a mouse model, and Res was administered by tube feeding to detect the serum biochemical liver function and inflammation levels, oxidative stress, and apoptosis in the livers of mice. An in vitro cellular model of liver inflammation and oxidative stress was established by treating mouse primary hepatocytes (MPHs) with tumor necrosis factor-α (TNF-α) and H 2 O 2 . The intrinsic mechanism of Res in attenuating hepatic inflammation and oxidative stress in CIA mice was explored by treating MPHs with an Nrf2 inhibitor and Keap1 overexpression plasmid. Results: Res significantly reduced the levels of inflammation and oxidative stress in liver tissues of CIA mice as well as in MPHs treated with TNF-α and H 2 O 2 and activated the Nrf2/Keap1 signaling pathway. Inflammation and oxidative stress levels in MPHs were exacerbated by the use of Nrf2 inhibitors and Keap1 overexpression, which promoted apoptosis. Conclusion: This study demonstrated the intrinsic mechanism of Res of attenuating hepatic inflammation and oxidative stress in CIA mice through the Nrf2/Keap1 pathway, which provides a new idea for finding hepatoprotective treatments for rheumatoid arthritis.
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Na Li,Hehe Shi,Wei Du,Siqian Luo,Xianyue Yang,Xinyue Yang,Bingyue Jiang,Peng Xia,Guangji Zhang,Wanghui Jing
The progression from ulcerative colitis to colitis-associated colorectal cancer (CAC) represents a significant clinical challenge. 6-Shogaol, a bioactive phenolic compound of ginger, exhibits anti-inflammatory, antioxidant, and anti-tumor properties. This study aims to investigate the therapeutic efficacy of 6-shogaol against colitis and CAC, and explore the underlying mechanisms through network pharmacology and in vivo validation. Putative hub targets and pathways associated with 6-shogaol were identified through network pharmacology. Murine models of dextran sulfate sodium (DSS)-induced colitis and azoxymethane/DSS-induced CAC were established, and the mice were treated with 6-shogaol to assess the latter’s therapeutic effects. The targets of 6-shogaol predicted through network pharmacology were mainly associated with oxidative stress and reactive oxygen species (ROS) signaling pathways. I n vivo , 6-shogaol relieved colitis symptoms and reduced CAC tumor burden. Furthermore, 6-shogaol alleviated intestinal inflammation by decreasing the colonic levels of TNF-α and MPO, and reduced oxidative stress in the colon tissues, as indicated by lower ROS production and malondialdehyde content. Moreover, 6-shogaol restored intestinal barrier function by upregulating claudin-4, occludin, and ZO-1, and decreasing intestinal permeability. Mechanistically, 6-shogaol promoted Nrf2 nuclear translocation by upregulating nuclear Nrf2 expression while downregulating cytoplasmic Keap1, thereby activating antioxidant response element driver genes, including Hmox1 , Nqo1 , and Gclc . Molecular docking confirmed strong binding affinity between 6-shogaol and Keap1 receptor, with a low binding energy of -6.89 kcal/mol. These findings collectively suggested that 6-shogaol alleviated colitis and CAC in murine models by inhibiting colonic inflammation, relieving oxidative stress, and enhancing intestinal barrier function through the activation of the Nrf2-Keap1 pathway.
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高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2023
·Vol. 24
·期 19
·14721
·
IF 5.6
Yue Wang,Shixiang Wei,Hui Lian,Lingling Tong,Linhui Yang,Bo Ren,Dongsheng Guo,He Huang
Ophiocordyceps gracilis(O. gracilis) is a parasitic fungus used in traditional Chinese medicine and functional foods. In this study, a neutral heteropolysaccharide (GSP-1a) was isolated from spores ofO. gracilis, and its structure and antioxidant capacities were investigated. GSP-1a was found to have a molecular weight of 72.8 kDa and primarily consisted of mannose (42.28%), galactose (35.7%), and glucose (22.02%). The backbone of GSP-1a was composed of various sugar residues, including →6)-α-D-Manp-(1→, →2,6)-α-D-Manp-(1→, →2,4,6)-α-D-Manp-(1→, →6)-α-D-Glcp-(1→, and →3,6)-α-D-Glcp-(1→, with some branches consisting of →6)-α-D-Manp-(1→ and α-D-Gal-(1→. In vitro, antioxidant activity assays demonstrated that GSP-1a exhibited scavenging effects on hydroxyl radical (•OH), 2,2′-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid radical cation (ABTS•+), and 2,2-diphenyl-1-picrylhydrazyl radical (DPPH•). Moreover, GSP-1a was found to alleviate H2O2-induced oxidative stress in HepG2 cells by reducing the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while enhancing the activities of superoxide dismutase (SOD). Furthermore, GSP-1a upregulated the mRNA expression of antioxidant enzymes such asHo-1,Gclm, andNqo1, and regulated the NRF2/KEAP1 and FNIP1/FEM1B pathways. The findings elucidated the structural types of GSP-1a and provided a reliable theoretical basis for its usage as a natural antioxidant in functional foods or medicine.Keywords:Ophiocordyceps gracilis;spores;polysaccharide;structural characterization;antioxidant activity
研究领域:
药理学
·
生物化学
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分子生物学
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传统中药
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DOI
PubMed
高影响因子
Food Bioscience
·
2026
·
IF 6.2
Qidong Xue,Kangning Li,Jie Mi,Dekun Cheng,Ruijie Liu,Ming Chang
Doxorubicin (Dox)-induced cardiotoxicity is a major dose-limiting adverse effect of chemotherapy and is closely linked to oxidative stress and impaired endogenous antioxidant defenses. Food-derived polyphenols that reinforce cellular redox resilience may therefore offer a safe adjuvant strategy. Pinus koraiensis nut skin (PNS), an underutilized nut-processing residue, is rich in polyphenols, yet its bioactive profile and cardioprotective mechanism remain insufficiently defined. Here, we optimized the extraction of PNS polyphenols (PNSP), profiled its phytochemical composition, and investigated its protective effects against Dox-induced cardiomyopathy (DIC). Under optimized conditions, PNSP exhibited strong in vitro antioxidant capacity. UPLC-Q-TOF-MS tentatively identified 26 phytochemicals dominated by procyanidins and flavonoids. In a zebrafish DIC model, post-treatment with PNSP (10 – 40 μg/mL) dose-dependently rescued cardiac dysfunction. Notably, 40 μg/mL PNSP restored heart rate from 112.00 ± 24.28 to 157.00 ± 13.98 beats/min and reduced ROS accumulation. Mechanistically, PNSP reactivated endogenous antioxidant enzymes (SOD, GSH-Px) by activating the Nrf2/Keap1 signaling pathway. Procyanidin C1 and the Pinus -specific flavonoid pinobanksin 3-acetate were identified as key ligands that competitively occupy the Keap1 Kelch pocket, thereby facilitating Nrf2 nuclear translocation. This non-covalent, competitive activation mechanism was robustly validated by molecular docking, stable Keap1 protein expression, and enhanced ARE-luciferase reporter activity. Collectively, these findings identify PNSP as a food-relevant Nrf2 activator with potential to mitigate chemotherapy-associated cardiotoxicity, highlighting its potential as a high-value functional food ingredient.
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DOI
高影响因子
Antioxidants
·
2020
·Vol. 9
·期 9
·783
·
IF 5.014
Bowen Sun,Xifan Wang,Xiaoxue Liu,Longjiao Wang,Fazheng Ren,Xiaoyu Wang,Xiaojing Leng
Chronic kidney disease (CKD) is characterized by the accumulation of protein-bound uremic toxins (PBUTs), which play a pathophysiological role in renal fibrosis (a common pathological process resulting in CKD progression). Accumulation of the PBUT hippuric acid (HA) is positively correlated with disease progression in CKD patients, suggesting that HA may promote renal fibrosis. Oxidative stress is the most important factor affecting PBUTs nephrotoxicity. Herein, we assessed the ability of HA to promote kidney fibrosis by disrupting redox homeostasis. In HK-2 cells, HA increased fibrosis-related gene expression, extracellular matrix imbalance, and oxidative stress. Additionally, reactive oxygen species (ROS)-mediated TGFβ/SMAD signaling contributed to HA-induced fibrotic responses. HA disrupted antioxidant networks by decreasing the levels of nuclear factor erythroid 2-related factor 2 (NRF2), leading to ROS accumulation and fibrotic responses, as evidenced by NRF2 activation and knockdown. Moreover, NRF2 levels were reduced by NRF2 ubiquitination, which was regulated via increased interactions of Kelch-like ECH-associated protein 1 with Cullin 3 and NRF2. Finally, renal fibrosis and redox imbalance promoted by HA were confirmed in rats. Importantly, sulforaphane (NRF2 activator) reversed HA-promoted renal fibrosis. Thus, HA promotes renal fibrosis in CKD by disrupting NRF2-driven antioxidant system, indicating that NRF2 is a potential therapeutic target for CKD.Keywords:hippuric acid;protein-bound uremic toxin;renal fibrosis;oxidative stress;antioxidation;NRF2;NRF2 ubiquitination
研究领域:
肾病学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
Frontiers in Physiology
·
2025
·
IF 3.4
Yi-Jia Liu,Jian Guo,Chang-Da Li,Si-Yin Han,Lu Cai
Introduction Intensive aquaculture frequently utilizes high-fat diets (HF) as a cost-effective strategy, yet this practice often induces hepatic steatosis, oxidative stress, and chronic inflammation in carnivorous fish. Betaine, a natural methyl donor, has shown potential as a functional feed additive, but its comprehensive protective mechanisms under HF stress remain to be fully elucidated. Methods Juvenile largemouth bass (Micropterus salmoides) were fed one of four isonitrogenous diets for 8 weeks: a normal-fat control (Control), a high-fat diet (HF), and two high-fat diets supplemented with 0.5% (HFB0.5) or 1.0% (HFB1) betaine. Growth performance, digestive enzyme activities, serum biochemical parameters, hepatic antioxidant capacity, and the expression of genes related to antioxidant defense, lipid metabolism, and inflammation were analyzed. Results The HF group exhibited significantly impaired growth, digestive function, and antioxidant capacity, along with elevated lipid peroxidation, dyslipidemia, and pro-inflammatory cytokine expression. Betaine supplementation restored growth performance and feed efficiency to control levels, ameliorated digestive enzyme activities (particularly enhancing lipase), and activated the hepatic Nrf2-Keap1 pathway, upregulating antioxidant genes (nrf2, sod1, cat, gpx, ho-1, gr) and enhancing enzyme activities. Betaine also improved serum lipid profiles, upregulated genes related to fatty acid oxidation (pparα, cpt-1) and lipolysis (lpl, hsl), suppressed lipogenic genes (srebp-1, fas), and rebalanced inflammatory cytokines by reducing tnf-α and il-1β while increasing tgf-β1 and il-10. Discussion Dietary betaine effectively counteracts HF-induced metabolic stress in M. salmoides through coordinated multi-pathway regulation. It enhances antioxidant defense, reprograms hepatic lipid metabolism toward catabolism, and restores inflammatory homeostasis. These findings underscore betaine’s role as a multi-functional feed additive capable of mitigating HF-related metabolic disorders and promoting overall health in carnivorous fish aquaculture.
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高影响因子
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