JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2025
·
IF 4.9
Jie Li,Bingyong Mao,Botao Wang,Xin Tang,Qiuxiang Zhang,Tianmeng Zhang,Jianxin Zhao,Hao Zhang,Shumao Cui
Luteolin (LUT) is a natural dietary ingredient with a wide range of biological functions and has been used in skin improvement. Skin lipid oversecreting is an exceedingly common disorder of the pilosebaceous glands and popular in adolescents. This study evaluated the effect of LUT on ameliorating oleic acid (OA) induced skin lipid accumulation in C57BL/6 mice and SZ95 cells. The level of major lipids and some key lipid metabolism markers were assessed, including triglyceride (TG), non-esterified fatty acid (NEFA), cholesterol, sterol regulatory-binding protein 1 and peroxisome proliferator-activated receptors. In vivo data showed decreasing significantly cholesterol levels and in vitro data demonstrated the remarkable influence in the reduction of TG and NEFA levels. Besides, LUT affected the diversity and structure of gut bacteria, an increase in the relative abundance of Akkermansia, Bacteroides and Alistipes , which were associated with the anti-oxidative and anti-inflammatory process. Additionally, our study presented that LUT significantly reduced the level of malondialdehyde (MDA, a lipid peroxidation marker), inhibited the expression of pro-inflammatory factor (TNF-α, IL-6) as well as up-regulated the mRNA expression level of SIRT1, indicating LUT alleviating inflammation and enhancing antioxidation may be associate with the activation of SIRT1 pathway.
研究领域:
皮肤病学
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药理学
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生物化学
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微生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
MOLECULAR MEDICINE
·
2024
·Vol. 30
·期 1
·1-16
·
IF 6
Xie Bin,Chen Qiong,Dai Ziyu,Jiang Chen,Chen Xi
Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease associated with high morbidity and mortality worldwide. Oxidative injury and mitochondrial dysfunction in the airway epithelium are major events in COPD progression.Methods and resultsThe therapeutic effects of Progesterone (P4) were investigated in vivo and in vitro in this study. In vivo, in a cigarette smoke (CS) exposure-induced COPD mouse model, P4 treatment significantly ameliorated CS exposure-induced physiological and pathological characteristics, including inflammatory cell infiltration and oxidative injury, in a dose-dependent manner. The c-MYC/SIRT1/PGC-1α pathway is involved in the protective function of P4 against CS-induced COPD. In vitro, P4 co-treatment significantly ameliorated H2O2-induced oxidative injury and mitochondrial dysfunctions by promoting cell proliferation, increasing mitochondrial membrane potential, decreasing ROS levels and apoptosis, and increasing ATP content. Moreover, P4 co-treatment partially attenuated H2O2-caused inhibition in Nrf1, Tfam, Mfn1, PGR-B, c-MYC, SIRT1, and PGC-1α levels. In BEAS-2B and ASM cells, the c-MYC/SIRT1 axis regulated P4’s protective effects against H2O2-induced oxidative injury and mitochondrial dysfunctions.Conclusion P4 activates the c-MYC/SIRT1 axis, ameliorating CS-induced COPD and protecting both airway epithelial cells and smooth muscle cells against H2O2-induced oxidative damage. PGC-1α and downstream mitochondrial signaling pathways might be involved.
研究领域:
呼吸病学
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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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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2021
·
IF 8.071
Wen Chen,Qiang Chu,Xiang Ye,Yuhao Sun,Yangyang Liu,Ruoyi Jia,Yonglu Li,Pengcheng Tu,Qiong Tang,Ting Yu,Chuan Chen,Xiaodong Zheng
Increasing attention has been brought to microplastics pollution recently, while emerging evidences indicate that nano-plastics degraded from microplastics are more of research significance owing to stronger toxicity. However, there is little study focused on the prevention of nano-plastics induced toxicity until now. Canidin-3-glucoside (C3G), a natural anthocyanin proved to possess multiple functions like antioxidant and intestinal tissue protection. Thus, we proposed whether C3G could act as a molecular weapon against nano-plastics induced toxicity. In Caco2 cell and Caenorhabditis elegans ( C. elegans ) models, we found that polystyrene (PS) nano-plastics exposure resulted in physiological toxicity and oxidative damage, which could be restored by C3G. More significantly in Caco2 cells, we observed that autophagy was activated via Sirt1-Foxo1 signaling pathway to attenuate PS induced toxicity after C3G intervention and further verified by adding autophagy inhibitor 3-Methyladenine (3-MA). Meanwhile, PS co-localization with lysosomes was observed, indicating the encapsulation and degradation of PS. In C. elegans , by detecting LGG-1/LC3 expression in GFP-targeted LGG-1 report gene (LGG-1:GFP) labeled transgenic DA2123 strain, the co-localization of LGG-1:GFP with PS was found as well, means that autophagy is involved in C3G’s beneficial effects. Furthermore, we were surprised to find that C3G could promote the discharge of PS from N2 nematodes, which reduces PS toxicity more directly.
研究领域:
环境科学
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毒理学
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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
Journal of Functional Foods
·
2026
·
IF 3.9
Yifan Zheng,Kunying Ding,Haojie Jin,Zhaorong Wang,Liujie Zheng,Zhengwei Fu,Yinhua Ni
Cellular senescence is a core hallmark of aging and a major risk factor for most chronic diseases. Natural products targeting senescent cells have garnered increasing attention for anti-senescence potential in aging-related disease intervention. Previous studies revealed that hydrolyzed chicken extract (HCE) exerts neuroprotective effects, but its role in senescent cell clearance and underlying mechanisms remains unclear. Here, we investigated the anti-senescent effects and mechanisms of HCE in D-galactose-induced senescent HT-22 hippocampal neurons, compared with the traditional essence of chicken (EC). HCE significantly enhanced cellular antioxidant capacity, reduced SA-β-gal positivity, restored cell cycle progression, inhibited senescence-associated secretory phenotype (SASP) secretion, and promoted autophagic flux, with a slightly stronger efficacy than EC. We further identified cyclo (Val-Pro), cyclo (His-Pro), and cyclo(Gly-Pro) as bioactive components, with cyclo(His-Pro) showing the strongest potency. Mechanistically, HCE and these cyclopeptides exerted effects via SIRT1/AMPK/mTOR-mediated autophagy, which was fully abolished by SIRT1 knockdown or targeted pathway inhibition.
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DOI
高影响因子
Animal Nutrition
·
2026
·
IF 8.3
Anran Wang,Jie Xu,Haoyue Guo,Dongxu Luo,Zhen Zhang,Chao Ran,Shuyan Miao,Zhigang Zhou
Fish oil is an essential lipid source in aquafeed due to its high polyunsaturated fatty acid content. However, its susceptibility to oxidation can harm aquatic animal health and growth. This study investigated the effects of oxidized fish oil (OFO) diet on hepatopancreas health of Macrobrachium rosenbergii , and the mechanism by which Cetobacterium somerae protects against oxidative damage induced by OFO diet. A total of 240 juvenile prawns (3.36 ± 0.02 g) were randomly allocated to three dietary treatments with four replicates of 20 prawns each for 8 weeks: Control (control diet with fresh fish oil diet), OFO (OFO diet), and OFO + Cet (OFO diet supplemented with C. somerae at 1.52 × 10 7 CFU/g). Compared with the OFO group, C. somerae intervention significantly reduced the levels of lipid peroxidation-related markers, including malondialdehyde (MDA), 5-hydroperoxyeicosatetraenoic acid (5-HETE), leukotriene B4 (LTB4), prostaglandins (PGs), and thromboxanes (TXs), while increasing hepatopancreatic antioxidant indicators, including total antioxidant capacity (T-AOC), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GSH-Px) ( P < 0.05). Moreover, it also reversed the OFO diet-induced alterations in the relative mRNA expression levels of ferroptosis-related genes ( acsl4 , tfr1 , gpx4 , and slc7a11 ) ( P < 0.05), potentially via the adenosine monophosphate (AMP)-activated protein kinase (AMPK)-sirtuin1 (SIRT1)-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signaling pathway. Serum acetic acid, a C. somerae metabolite, exhibited the most pronounced alteration in the C. somerae -treated group ( P = 0.004). Furthermore, 160 juvenile prawns (2.62 ± 0.12 g) were randomly divided into two groups with four replicates of 20 prawns in each for 4 weeks: OFO diet, OFO + 0.15% sodium acetate (0.15% NaAc). Supplementation with 0.15% NaAc in the OFO diet also effectively decreased the peroxides (MDA, 5-HETE, LTB4, and TXs) and reversed the OFO diet-induced alterations in the relative mRNA expression levels of ferroptosis-related genes ( acsl4 , tfr1 , gpx4 , and slc7a11 ) compared with OFO group ( P < 0.05), suggesting a contributory role of acetate in the functionality of C. somerae . Meanwhile, the elevated AMP/adenosine triphosphate (ATP) ratio and upregulated relative mRNA expression levels of acss1/2 , ampk, sirt1 , and pgc-1α ( P < 0.05) indicated that C. somerae- derived acetate activates AMP production, thereby activating the AMPK-SIRT1-PGC-1α signaling pathway . Overall, C. somerae protects against OFO diet-induced hepatopancreatic injury by mitigating ferroptosis via acetate-mediated activation of the AMPK-SIRT1-PGC-1α signaling pathway.
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DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2022
·
IF 5.714
Yaojian Rao,Junjie Li,Ruofei Qiao,Jinxin Luo,Yan Liu
Background Both Tetramethylpyrazine (TMPZ) and Astragaloside IV (AGS-IV) can ameliorate neuronal apoptosis and neuroinflammation in CNS diseases. This study revolves around the underlying mechanism of TMPZ and AGS-IV in spinal cord injury (SCI)-associated neuropathic pain (NP). Materials and methods An in-vivo NP model was constructed in Sprague-Dawley (SD) rats via SCI. qRT-PCR was employed to detect OIP5-AS1 and miR-34a. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) of the rats were evaluated. Neuronal apoptosis in the spinal cord of rats was examined by Nissl staining and TUNEL staining. The interactions between OIP5-AS1 and miR-34a as well as miR-34a and Sirt1 were investigated through dual luciferase assay and RIP assay. The protein expressions of Bad, Bax, Caspase-3, iNOS, COX2, NF-κB, and Sirt1 were examined by western blot. Results TMPZ and AGS-IV combination relieved behavioral symptoms of neuropathic pain in the SCI rat model, enhanced the levels of OIP5-AS1 and Sirt1, and lowered the profile of miR-34a. OIP5-AS1 downregulation weakened the neuroprotective function of TMPZ and AGS-IV in SCI rats and reversed their anti-inflammatory and anti-apoptotic effects on LPS-elicited primary spinal cord neurons. miR-34a was identified as a target of OIP5-AS1. Upregulated miR-34a partly abated the protective functions of TMPZ and AGS-IV in primary spinal cord neurons. Additionally, miR-34a targeted and repressed Sirt1, thus activating the NF-κB pathway and inflammatory reactions. Sirt1 inhibition reduced the protective effects mediated by OIP5-AS1. Conclusion TMPZ and AGS-IV ameliorate SCI-elicited NP via the OIP5-AS1/miR-34a/Sirt1/NF-κB pathway.
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DOI
PubMed
高影响因子
JOURNAL OF PINEAL RESEARCH
·
2023
·
IF 10.3
Chao Gu,Quan Zhou,Xiayu Hu,Xiaoyang Ge,Mingzhuang Hou,Wenhao Wang,Hao Liu,Qin Shi,Yong Xu,Xuesong Zhu,Huilin Yang,Xi Chen,Tao Liu,Fan He
Osteoporotic bone defects, a severe complication of osteoporosis, are distinguished by a delayed bone healing process and poor repair quality. While bone marrow-derived mesenchymal stem cells (BMMSCs) are the primary origin of bone-forming osteoblasts, their mitochondrial function is impaired, leading to inadequate bone regeneration in osteoporotic patients. Melatonin is well-known for its antioxidant properties and regulation on bone metabolism. The present study postulated that melatonin has the potential to enhance the repair of osteoporotic bone defects by restoring the mitochondrial function of BMMSCs. In vitro administration of melatonin at varying concentrations (0.01, 1, and 100 μM) demonstrated a significant dose-dependent improvement in the mitochondrial function of BMMSCs obtained from ovariectomized rats (OVX-BMMSCs), as indicated by an elevation in mitochondrial membrane potential, adenosine triphosphate synthesis and expression of mitochondrial respiratory chain factors. Melatonin reduced the level of mitochondrial superoxide by activating the silent information regulator type 1 (SIRT1) and its downstream antioxidant enzymes, particularly superoxide dismutase 2 (SOD2). The protective effects of melatonin were found to be nullified upon silencing of Sirt1 or Sod2 , underscoring the crucial role of the SIRT1-SOD2 axis in the melatonin-induced enhancement of mitochondrial energy metabolism in OVX-BMMSCs. To achieve a sustained and localized release of melatonin, silk fibroin scaffolds loaded with melatonin (SF@MT) were fabricated. The study involved the surgical creation of bilateral femur defects in OVX rats, followed by the implantation of SF@MT scaffolds. The results indicated that the application of melatonin partially restored the mitochondrial energy metabolism and osteogenic differentiation of OVX-BMMSCs by reinstating mitochondrial redox homeostasis. These findings suggest that the localized administration of melatonin through bone implants holds potential as a therapeutic approach for addressing osteoporotic bone defects.
研究领域:
药理学
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干细胞生物学
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骨再生
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组织工程
·
骨质疏松
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DOI
PubMed
高影响因子
Cell Metabolism
·
2024
·
IF 27.7
Yu Jiang,Yawen Wang,Guofeng Chen,Fei Sun,Qijing Wu,Qiong Huang,Dongqiang Zeng,Wenjun Qiu,Jiao Wang,Zhiqi Yao,Bishan Liang,Shaowei Li,Jianhua Wu,Na Huang,Yuanyuan Wang,Jingsong Chen,Xiaohui Zhai,Li Huang,Beibei Xu,Masami Yamamoto,Tetsuya Tsukamoto,Sachiyo Nomura,Wangjun Liao,Min Shi
Immune checkpoint blockade has led to breakthroughs in the treatment of advanced gastric cancer. However, the prominent heterogeneity in gastric cancer, notably the heterogeneity of the tumor microenvironment, highlights the idea that the antitumor response is a reflection of multifactorial interactions. Through transcriptomic analysis and dynamic plasma sample analysis, we identified a metabolic “face-off” mechanism within the tumor microenvironment, as shown by the dual prognostic significance of nicotinamide metabolism. Specifically, macrophages and fibroblasts expressing the rate-limiting enzymes nicotinamide phosphoribosyltransferase and nicotinamide N-methyltransferase, respectively, regulate the nicotinamide/1-methylnicotinamide ratio and CD8+ T cell function. Mechanistically, nicotinamide N-methyltransferase is transcriptionally activated by the NOTCH pathway transcription factor RBP-J and is further inhibited by macrophage-derived extracellular vesicles containing nicotinamide phosphoribosyltransferase via the SIRT1/NICD axis. Manipulating nicotinamide metabolism through autologous injection of extracellular vesicles restored CD8+ T cell cytotoxicity and the anti-PD-1 response in gastric cancer.
研究领域:
肿瘤学
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免疫学
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代谢学
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癌症生物学
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DOI
PubMed
高影响因子
Antioxidants
·
2024
·Vol. 13
·期 7
·859
·
IF 6
Ruifeng Wang,Anping Ding,Jiaye Wang,Jiaxue Wang,Yujie Zhou,Miao Chen,Shuang Ju,Mingpu Tan,Zengxu Xiang
Astragalin (AG), a typical flavonoid found inThesium chinenseTurcz (T. chinense), is abundant in various edible plants and possesses high nutritional value, as well as antioxidant and antibacterial effects. In this study, we initially predicted the mechanism of action of AG with two anti-aging and antioxidant-related protein targets (CD38 and IGFR) by molecular docking and molecular dynamics simulation techniques. Subsequently, we examined the anti-aging effects of AG inCaenorhabditis elegans(C. elegans), the antioxidant effects in zebrafish, and verified the related molecular mechanisms. InC. elegans, AG synergistically extended the lifespan ofC. elegansby up-regulating the expression ofdaf-16through inhibiting the expression ofdaf-2/IGFRand also activating the AMPK and MAPK pathways to up-regulate the expression ofsir-2.1,sir-2.4, andskn-1. In oxidatively damaged zebrafish embryos, AG demonstrated a synergistic effect in augmenting the resistance of zebrafish embryos to oxidative stress by up-regulating the expression levels ofSIRT1andSIRT6within the zebrafish embryos system via the suppression of CD38 enzymatic activity and then inhibiting the expression ofIGFRthrough high levels ofSIRT6. These findings highlight the antioxidant and anti-aging properties of AG and indicate its potential application as a supplementary ingredient in aquaculture for enhancing fish health and growth.
研究领域:
分子生物学
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老年医学
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营养科学
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水产养殖
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2024
·Vol. 22
·期 1
·1-19
·
IF 10.6
Jiang Mingzhou,Zhu Zhidong,Zhou Ziyu,Yan Zhiqiang,Huang Kai,Jiang Rongrong,Fan Xi,Jieensi Milayi,Pang Liewen,Wang Yiqing,Sun Xiaotian
Background Cardiovascular events secondary to stroke–collectively classified as stroke-heart syndrome–greatly impair the patient’s prognosis, however its underlying mechanism has yet to be determined. To investigate the mechanism of central neuroinflammation and its effects on stroke-heart syndrome, a temperature-ultrasound responsive brain-targeted drug delivery system, DATS/MION-LPE, was synthesized to specifically study neuroinflammation in the mouse middle cerebral artery occlusion (MCAO) model.Results The specific polymer of DATS/MION-LPE can close the nanoparticle pores at 37 °C, restricting drug release in the circulation. After the nanoparticles were targeted to brains, the polymer can be cleaved under external ultrasound irradiation, reopening the nanoparticle pores and allowing drug release, therefore directly managing the neuroinflammation. After a stroke, a significant cerebral inflammation occurred, with elevated IL-1β and pyrin domain-containing 3 (NLRP3) inflammasome. Accordingly, significantly increased histone deacetylase 6 (HDAC6) and decreased sirtuin 1 (SIRT1) were observed. An antagonistic relationship between HDAC6 and SIRT1 was found, which can jointly regulate the cerebral NLRP3 expression. The systemic IL-1β and ATP levels were increased after the stroke, accompanied by a significant heart injury including contractile dysfunction, elevated IL-1β levels, and oxidative stress. Meanwhile, neuroinflammation can trigger sympathetic nervous overexcitation with associated heart damage. DATS/MION-LPE can targetedly effect on ischemic brain, exhibiting cerebral and cardiac protective effects including downregulated cerebral NLRP3 and HDAC6 expressions, upregulated SIRT1 expressions in brain, reduced IL-1β and ATP in circulation, and alleviated cardiac impairment.Conclusion This study introduced the key role of neuroinflammation in stroke-heart syndrome and first investigated the crucial HDAC6/SIRT1-NLRP3 circuit in this process. Heart injury secondary to stroke is mediated by neuroinflammation induced systemic inflammatory responses and sympathoexcitation. DATS/MION-LPE is a unique tool and effective therapeutic agent, which provides new insights into combinational heart and cardiac protection.Graphical Abstract
研究领域:
神经科学
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心血管疾病
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药物递送系统
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炎症
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分子生物学
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产品关联
DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2024
·
IF 5.4
Yan Wang,Jialiang Lin,Zihao Yu,Jinbo Cheng,Jianhua Cheng,Weikang Cui
Peptides are recognized as highly effective and safe bioactive ingredients. However, t their practical application is limited and hampered by harsh conditions for practical drug delivery. Hence, a novel peptide nanocarrier of copper peptide (GHK-Cu) encapsulation developed by liposome technology combined with the classical Chinese concept of rigidity and flexibility. Different polyols were selected as modification ligands for phospholipid bilayers to construct a nano drug-carrying system with high loading rate, good stability and biocompatibility. In vitro, this complex not only significantly retarded the release ability of copper peptides, but also enabled copper peptides to be effectively resistant to enzymatic degradation. Furthermore, cellular experiments showed that this system mainly regulates Nrf2, SIRT1, and PEG2/COX-2-related signaling pathways, thus effectively counteracting cellular inflammation, senescence, and apoptosis from oxidative damage. Interestingly, a green, non-toxic, efficient and convenient antioxidant system was developed for the prevention and deceleration of skin aging.
研究领域:
药剂学
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纳米技术
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皮肤病学
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生物化学
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产品关联
DOI
PubMed
高影响因子
ACS Biomaterials Science & Engineering
·
2024
·
IF 5.4
Yixiao Chen,Guoqing Li,Yufeng Ge,Su Liu,Jian Weng,Jianjing Lin,Ao Xiong,Hui Zeng,Xinbao Wu,Jun Yang,Fei Yu
In this study, we explore the cartilage defect repair mechanism by phosphocreatine-grafted chitosan hydrogels loaded with berberine-treated ATDC5 cells (CSMP@BBR@ATDC5). Under the optimal concentrations of LPS and BBR ideal conditions, ATDC5 cell toxicity and proliferation were detected with AM/PI and EdU staining. Additionally, qPCR and Western blot were employed to detect the expression of the SIRT1/BMP4 signaling pathway and chondrogenic-related factors in ATDC5 cells. Moreover, BBR-treated ATDC5 was seeded into a phosphocreatine-grafted chitosan hydrogel system. Subsequently, the cartilage defect was established in mice. After 4, 8, and 12 weeks, knee specimens were collected to evaluate the repair of cartilage defects. According to our findings, BBR can increase ATDC5 viability by LPS treatment. Likewise, it upregulates the SIRT1/BMP4 signaling pathway expression and chondrogenic-related factors. Another, it was shown by histological observation that the cartilage defect had been repaired more effectively in the CSMP@BBR@ATDC5 group than in the other groups. Finally, the expressions of chondrogenic-related factors and SIRT1/BMP4 signaling pathway were upregulates in CSMP@BBR@ATDC5 than in other groups. In vitro, BBR protects inflammatory ATDC5 cells and maintains the expression of chondrogenic-related factors. Subsequently, we successfully use CSMP@BBR@ATDC 5 to repair knee cartilage defects in mice.
研究领域:
组织工程
·
再生医学
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骨科
·
细胞生物学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）