MOLECULAR NUTRITION & FOOD RESEARCH
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2024
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IF 4.5
Mengcheng Jin,Tangbin Zou,Hairong Huang,Ming Chen,Haoqi Zou,Baoyan Chen,Chengze Lai,Huawen Li,Peiwen Zhang
Scope Bile acids play a crucial role in lipid absorption and the regulation of lipid, glucose, and energy homeostasis. Coenzyme Q10 (CoQ10), a lipophilic antioxidant, has been recognized for its positive effects on obesity and related glycolipid metabolic disorders. However, the relationship between CoQ10 and bile acids has not yet been evaluated. Methods and results This study assesses the impact of CoQ10 treatment on bile acid metabolism in mice on a high-fat diet using Ultra-Performance Liquid Chromatography-tandem Mass Spectrometry. CoQ10 reverses the reduction in serum and colonic total bile acid levels and alters the bile acid profile in mice that are caused by a high-fat diet. Seventeen potential targets of CoQ10 in bile acid metabolism are identified by network pharmacology, with six being central to the mechanism. Molecular docking shows a high binding affinity of CoQ10 to five of these key targets. Further analyses indicate that farnesoid X (FXR) receptor and Takeda G-protein coupled receptor 5 (TGR5) may be crucial targets for CoQ10 to regulate bile acid metabolism and exert beneficial effects. Conclusion This study sheds light on the impact of CoQ10 in bile acids metabolism and offers a new perspective on the application of CoQ10 in metabolic health.
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Drug Design Development and Therapy
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2026
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IF 6.1
Liwei Feng,Linjie Tian,Jing Guo,Lingling Zhang,Peng Wang,Xiaolin Bu
Introduction Ultraviolet B (UVB) irradiation is a key exogenous factor contributing to skin photoaging. Idebenone (IDE), a structural analog of coenzyme Q10 (CoQ10), exhibits potent free radical scavenging capacity and is mainly employed in the treatment of neurodegenerative disorders, and in anti-aging products. However, the molecular mechanisms underlying its photoprotective effects in skin cells remain poorly understood.Purpose This study aims to investigate the protective effects of IDE against UVB-induced photoaging in human immortalized epidermal keratinocytes (HaCaT cells).Methods We applied IDE to a UVB-induced HaCaT cell photoaging model and found that it significantly ameliorated the photoaging damage caused by UVB irradiation.Results Specifically, cell morphology recovered from a shrinkage state toward normal, the positivity rate of senescence-associated β-galactosidase (SA-β-gal) decreased, and enhanced the impaired cell migration and proliferation capacities. Additionally, oxidative stress imbalance was alleviated, as evidenced by a significant reduction in reactive oxygen species (ROS) and malondialdehyde (MDA) levels, along with an increase in superoxide dismutase (SOD) activity. Impaired mitochondrial function was restored, reflected by the repolarization of mitochondrial membrane potential (MMP) and an increase in adenosine triphosphate (ATP) synthesis. Furthermore, the elevated secretion levels of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-8 (IL-8) were significantly reduced. Transcriptomic analysis and protein validation revealed that IDE significantly downregulated the expression of IL-3RA and effectively restored the expression of TUBA8.Conclusion IDE significantly improved UVB-induced photoaging damage in HaCaT cells through multiple pathways, including restoring cell viability, alleviating oxidative stress damage, reducing pro-inflammatory factor infiltration, and protecting mitochondrial function. Its mechanism of action may involve the regulation of targets such as IL-3RA and TUBA8.
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CURRENT EYE RESEARCH
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2026
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IF 1.7
Rujun He,Wei Ding,Juan Cao,Cong Guo,Xu Li,Guohua Xiao
Purpose To evaluate ergothioneine (EGT), a naturally occurring amino acid and endogenous antioxidant, as a novel therapeutic agent for oxidative stress-related ocular diseases. This evaluation specifically aimed to address the challenge of targeted ocular delivery by assessing EGT’s antioxidant potency, stability, ocular tolerance, and crucially, its ability to reach the posterior segment (fundus) via topical administration.Methods This study evaluated EGT as a novel ocular antioxidant by examining its radical scavenging capacity (DPPH assay compared to glutathione, astaxanthin, and coenzyme Q10), stability (at 40 °C/75% relative humidity for six months using HPLC), ocular tolerance (using a New Zealand rabbit model), and fundus delivery efficiency (topical D9-EGT eye drops quantified by LC-MS/MS).Results EGT demonstrated significantly superior radical scavenging activity, exhibiting 6.4-fold and 46-fold higher rates than glutathione and coenzyme Q10, respectively, at 50 ppm. It also showed excellent stability, retaining over 97% of its initial concentration after six months, and caused no ocular irritation at any tested concentration (score 0). Importantly, topical administration of EGT resulted in effective fundus delivery, with peak concentrations reached at 0.5 h post-application (1181 ± 56 ng/g), confirming successful penetration through corneal and scleral barriers. These findings establish EGT as a potent, multi-mechanistic antioxidant characterized by high stability, ocular safety, and exceptional posterior segment penetrance via noninvasive eye drops.Conclusion These findings establish EGT as a potent, multi-mechanistic antioxidant characterized by high stability, ocular safety, and exceptional posterior segment penetrance via noninvasive eye drops. By overcoming key delivery limitations, EGT presents a promising therapeutic strategy for oxidative stress-related ocular diseases such as age-related macular degeneration and diabetic retinopathy. Further studies are warranted to evaluate its long-term efficacy and clinical translation potential.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Xiao-jiang Mao,Xue-shan Li,Ling Wang,Kai Song,Chun-xiao Zhang,Ke-Quan Chen,Kang-le Lu
Coenzyme Q10 (COQ10), a natural fat-soluble compound, is known to protect mitochondria, though the exact mechanism remains unclear. Here, we explored the mechanism through which COQ10 enhances mitochondrial function using hepatocytes from spotted seabass ( Lateolabrax maculatus ). Three experimental groups were established: a normal medium control group, a fatty acid (FA) group containing 100 μM FA, and a group containing100 μM FA plus 5 μM COQ10 (FA + COQ10). After incubation, the results showed that FA treatment significantly increased triglyceride content in the cells, while COQ10 treatment reduced triglycerides content ( P < 0.05). Additionally, COQ10 alleviated FA-induced hepatocyte damage, restored mitochondrial membrane potential and increased ATP content ( P < 0.05). Further analysis showed that FA downregulated key mitophagy genes ( PINK1 , PARKIN , and LC3B ) while upregulating P62 ( P < 0.05). To investigate whether the enhancement of mitochondrial function by COQ10 is dependent on mitophagy activation, we used the mitophagy inhibitor Mdivi-1 and set it to FA + COQ10 + Mdivi-1 group. After mtphagy Dye staining, the number of autophagosomes in the FA + COQ10 + Mdivi-1 group was lower than in the FA + COQ10 group, indicating that the mitophagy activation by COQ10 was inhibited. Overall, these results demonstrated that COQ10 enhances mitochondrial function and alleviates excessive fat deposition in hepatocytes via PINK1-mediated mitophagy. This also indicates that COQ10 can be potentially applied to improve the metabolic disorders of fish in aquaculture.
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BIORESOURCE TECHNOLOGY
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2025
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IF 9
Xinru Bao,Jie Zhong,Zikang Huang,Guangyi Xiao,Qiaomin Yang,Wenkang Yu,Bingmei Wang,Wenjin He,Naipeng Kan,Jianzhong Huang,Feng Qi
Coenzyme Q10 (CoQ 10 ), a lipid-soluble isoprenylated benzoquinone essential for electron transfer, is synthesized in the inner mitochondrial membrane of eukaryotes and plasma membrane of prokaryotes like Rhodobacter sphaeroides . Despite its natural production capacity, industrial-scale CoQ 10 synthesis remains limited by ineffective metabolic regulation and scarce genetic tools in R. sphaeroides . This study investigated the relationship between CoQ 10 and intracellular lipid accumulation to enhance production. The engineered strains with higher cardiolipin (CL) levels showed enlarged membrane surfaces, synergistically increasing CoQ 10 production. However, increased triacylglycerol (TAG) accumulation reduced CoQ 10 yields. Disrupting phospholipase D (PLD) and lysophospholipase (PLDB) genes, which reduce phospholipid hydrolysis, further improved CoQ 10 biosynthesis. The optimized strain RS-SQCL04, incorporating all the effective strategies, achieved 824 mg/L CoQ 10 via fed-batch fermentation, a 57.9 % increase over the control. This study provides a promising strategy for industrial CoQ 10 production through phospholipid engineering in R. sphaeroides .
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ADVANCED FUNCTIONAL MATERIALS
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2023
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IF 19
Tiantian Chen,Yan Qin,Yao Li,Yaru Li,Jiajia Luo,Lanlan Fan,Meiyu Feng,Zheng Wang,Yanjun Zhao
The dose-dependent cardiomyopathy of adriamycin (doxorubicin) limits its long-term clinical use, which is revealed as a consequence of cardiomyocyte ferroptosis. As a ferrous iron (Fe 2 + )-dependent regulated cell death pathway, ferroptosis is induced by the tailored lipid peroxides in the cell membranes. Herein, iron-chelating polymer micelles are reported for concurrent doxorubicin delivery and cardiotoxicity reduction. The amphiphilic polymer consists of methoxy poly (ethylene glycol)- co -poly (glutamic acid) copolymer as the backbone and deferiprone analog as the side chain. The chiral polymer adopted the α-helix conformation to enable prolonged retention in the cell membranes, resulting in efficient iron chelation, ferroptosis inhibition, and cardiotoxicity reduction. The co-encapsulation of doxorubicin and coenzyme Q 10 (CoQ 10 ) in micelles further alleviates the cardiotoxicity because the reduced CoQ 10 can act as a radical trapping agent to constrain lipid peroxidation and cardiomyocyte ferroptosis. The reduction of cardiotoxicity is accompanied by enhanced anticancer efficacy in an in vivo murine breast cancer model. The chiral iron-chelating polymer micelles can be a promising platform for enhanced doxorubicin delivery and reduced cardiac adverse effects.
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JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
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2023
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IF 5
Shuoye Yang,Yakun Niu,Siqi Li,Mingzhen Lv,Jiaxin Liu,Lu Zhang,Lan Cui,Lingbo Qu
Coenzyme Q10 (CoQ10) has a wide range of nutraceutical functions and therapeutic values, nevertheless, its biomedical application as a health product or drug is hampered by the low absorption efficiency and bioavailability. In the present study, the hybrid mesoporous silica nanoparticle-supported lipid bilayers (LMSNs) as nanocarriers for CoQ10 are prepared by fusing the phospholipid membrane onto MSNs cores. Further, LMSNs are functionalized with d -α-tocopherol polyethylene glycol 1000 succinate (TPGS), deoxycholic acid (Doca) and chitosan (CS) sequentially, to obtain the TPGS-LMSNs and DCs-TPGS-LMSNs samples, respectively. MSNs, liposomes , and unmodified LMSNs are also prepared as controls. The results reveal that various nanocarriers have a high loading capacity for CoQ10, low cytotoxicity towards Caco-2 cells, and sustained release property in different pH mediums. In contrast to other nano-formulations, [email protected] show the higher cellular uptake efficiency and the resulting ROS inhibition effect, which can be taken up by cells via caveolae-mediated route, macropinocytosis, and unique bile acid uptake pathway mediated by ASBT. Efficient delivery of DC-TPGS-LMSNs is further illustrated by in vivo intestinal uptake and pharmacokinetics study, in which [email protected] exhibit higher absorption efficiency, longer circulation time, and more enhanced bioavailability than other formulations after oral administration. The results suggest that multifunctional LMSNs might be the potent candidate for CoQ10 delivery, and the findings will contribute to the rational design of novel drug delivery vehicles .
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FOOD CHEMISTRY
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2022
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IF 9.231
Yaqin Wang,Lingjia Fan,Jintao Huang,Jingjing Liang,Xingnan Wang,Yichen Ren,Hongcai Li,Tianli Yue,Zhenpeng Gao
To prepare pumpkin juice (PJ) rich in coenzyme Q10, this study analyzed the chemical composition, antioxidant activity, and gut microbiota of pumpkin juice fermented by Rhodobacter sphaeroides (RPJ). The number of viable bacteria in the juice reached 2.8 × 10 8 CFU/mL; the fermentation process mainly consumed glucose and sucrose; the total sugar content was reduced, β -carotene was reduced, and a new antioxidant substance, coenzyme Q10, appeared at a content of 12.345 mg/L; levels of volatile alcohols, esters, and ketones significantly increased; and antioxidation ability improved, particularly the ferric ion reducing antioxidant power activity. The gut microbiota of mice shifted by increasing Lactobacillus and Bifidobacterium and protected the gut barrier by reducing Proteobacteria after 48 h of fermentation. Pumpkin juice fermented by Rhodobacter sphaeroides not only produces bioactive substances with antioxidant capacity but can also regulate the gut microbiota of mice.
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2022
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IF 3.322
Xuan Ma,Hui Chen,Lixing Cao,Shuang Zhao,Chong Zhao,Shutao Yin,Lihong Fan,Hongbo Hu
Ferroptosis is a new form of iron-dependent cell death . A growing body of evidence suggests that abnormal ferroptosis is involved in developing neurodegenerative diseases. 18β-glycyrrhetinic acid (GA) is a major bioactive component of licorice with multiple biological activities including neuroprotection. Give the role of ferroptosis in the neurodegenerative diseases, we hypothesized that the neuroprotective effect of GA might be associated with its ability to protect neuro-cells from ferroptosis. Results demonstrated that GA was able to prevent a well-known ferroptosis inducer ferroptosis inducer 56 (FIN56)-triggered ferroptosis in HT22 mouse neuronal cell. Further mechanistic investigation revealed that the protection of GA on ferroptosis is attributed its inhibiting effect on cellular labile iron accumulation and up-regulating coenzyme Q10 (CoQ10) levels. The findings of the present study uncovered a novel mechanism involved in the neuroprotective effect of GA, and imply that GA could be developed as a novel agent to manage ferroptosis-related diseases.
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BIOMEDICINE & PHARMACOTHERAPY
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2022
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IF 7.419
Mohsen Sheykhhasan,Razieh Amini,Sara Soleimani Asl,Massoud Saidijam,Seyed Mahmoud Hashemi,Rezvan Najafi
Alzheimer's disease (AD) is a degenerative disease that causes memory and learning impairments as well as dementia. Coenzyme Q10 (CoQ10) is an anti-inflammatory and anti-oxidative stress supplement that can improve inflammation and oxidative stress associated with AD. This study investigated the effects of drug delivery of COQ10 by exosomes derived from adipose-derived stem cells (ADSCs-Exo) on cognition, memory, and neuronal proliferation in a rat model of Streptozotocin (STZ)-induced AD. Since the establishment of the AD model, the rats have received intraperitoneal injections of CoQ10, Exo, or CoQ10-loaded ADSCs-Exo (Exo+ CoQ10). The passive avoidance test and the Morris water maze (MWM) were used to assess memory and cognition changes. Cell density was determined using histological methods. The expression of BDNF was measured using an ELISA kit. SOX2 expression was determined using immunohistochemistry. According to the results of the MWM and passive avoidance task, Exo+CoQ10 significantly improved STZ-induced memory impairment compared to CoQ10 and Exo groups alone. Furthermore, BDNF expression increased in the STZ-induced rats after Exo+ CoQ10, when compared to the CoQ10 and Exo groups. In addition, Exo+CoQ10 had the highest cell density and SOX2 gene expression, when compared to the CoQ10 and Exo groups. According to the findings of this study, Exo+ COQ10 enhanced cognition and memory deficiency in Alzheimer's disease by boosting BDNF and SOX2 levels in the hippocampus. Hence, the use of exosomes derived from adipose-derived stem cells as the carrier of CoQ10 may increase the therapeutic effect of CoQ10, which can possibly be due to the regenerative properties of the exosomes.
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Journal of Translational Medicine
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2023
·Vol. 21
·期 1
·1-23
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IF 7.4
Yuan Shun,Che Yanjia,Wang Zhiwei,Xing Kai,Xie Xiaoping,Chen Yuanyang
Background Heart transplantation (HT) has been approved as an optimal therapeutic regimen for patients with terminal-stage cardiac failure. However, cold ischaemia‒reperfusion (I/R) injury remains an unavoidable and outstanding challenge, which is a major factor in early graft dysfunction and an obstacle to long-term survival in HT. Cold I/R injury induces cardiac graft injury by promoting mitochondrial dysfunction and augmenting free radical production and inflammatory responses. We therefore designed a mitochondrion-targeted nanocarrier loaded with Coenzyme Q10 (CoQ10) (CoQ10@TNPs) for treatment of cold I/R injury after cardiac graft in a murine heterotopic cardiac transplantation model.Methods Hybrid nanoparticles composed of CaCO3/CaP/biotinylated-carboxymethylchitosan (CaCO3/CaP/BCMC) were synthesized using the coprecipitation method, and the mitochondria-targeting tetrapeptide SS31 was incorporated onto the surface of the hybrid nanoparticles through biotin-avidin interactions. Transmission electron microscopy (TEM) and dynamic light scattering (DLS) analysis were used for characterisation. In vitro, the hypoxia-reoxygenation model of H9c2 cells was employed to replicate in vivo cold I/R injury and treated with CoQ10@TNPs. The impact of CoQ10@TNPs on H9c2 cell injury was assessed by analysis of oxidative damage and apoptosis. In vivo, donor hearts (DHs) were perfused with preservation solution containing CoQ10@TNPs and stored in vitro at 4 °C for 12 h. The DHs were heterotopically transplanted and analysed for graft function, oxidative damage, apoptosis, and inflammatory markers 1 day post-transplantation.Results CoQ10@TNPs were successfully synthesized and delivered CoQ10 to the mitochondria of the cold ischaemic myocardium. In vitro experiments demonstrated that CoQ10@TNPs was taken up by H9c2 cells at 4 °C and localized within the mitochondria, thus ameliorating oxidative stress damage and mitochondrial injury in cold I/R injury. In vivo experiments showed that CoQ10@TNPs accumulated in DH tissue at 4 °C, localized within the mitochondria during cold storage and improved cardiac graft function by attenuating mitochondrial oxidative injury and inflammation.Conclusion sCoQ10@TNPs can precisely deliver CoQ10 to the mitochondria of cold I/R-injured cardiomyocytes to effectively eliminate mitochondrial reactive oxygen species (mtROS), thus reducing oxidative injury and inflammatory reactions in cold I/R-injured graft tissues and finally improving heart graft function. Thus, CoQ10@TNPs offer an effective approach for safeguarding cardiac grafts against extended periods of cold ischaemia, emphasizing the therapeutic potential in mitigating cold I/R injury during HT. These findings present an opportunity to enhance existing results following HT and broaden the range of viable grafts for transplantation.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2023
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IF 6.1
Xiang Luo,Sha Ao,Hongze Wu,David Julian McClements,Likun Fang,Mengyu Huang,Yanyan Zhou,Xuguang Yin,Meiyang Xi,Tao Cai,Kewu Zhu
Fish oils are a rich source of polyunsaturated fatty acids, including eicosapentaenoic acid and docosahexaenoic acid, which are reported to exhibit therapeutic effects in a variety of human diseases. However, these oils are highly susceptible to degradation due to oxidation, leading to rancidity and the formation of potentially toxic reaction products. The aim of this study was to synthesize a novel emulsifier (HA-PG10-C18) by esterifying hyaluronic acid with poly(glyceryl)10-stearate (PG10-C18). This emulsifier was then used to formulate nanoemulsion-based delivery systems to co-deliver fish oil and coenzyme Q10 (Q10). Q10-loaded fish oil-in-water nanoemulsions were fabricated, and then their physicochemical properties, digestibility, and bioaccessibility were measured. The results indicated that the environmental stability and antioxidant activity of oil droplets coated with HA-PG10-C18 surpassed those coated with PG10-C18 due to the formation of a denser interfacial layer that blocked metal ions, oxygen, and lipase. Meanwhile, the lipid digestibility and Q10 bioaccessibility of nanoemulsions formulated with HA-PG10-C18 (94.9 and 69.2%) were higher than those formulated with PG10-C18 (86.2 and 57.8%), respectively. These results demonstrated that the novel emulsifier synthesized in this study could be used to protect chemically labile fat-soluble substances from oxidative damage, while still retaining their nutritional value.
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