MICROCHEMICAL JOURNAL
·
2019
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IF 3.206
Guohan Sun,Shiqiao Wang,Jianfeng Zhou,Jianbin Pan,Yanli Tong,Qinghua Mei,Haiyun Zhai
In the present study, a novel and facile poly-m-amino-benzenesulfonic acid (p-m-ABSA) film on glassy carbon electrode (GCE) was developed using pulse potentiostatic method (PPM), which is employed with the oxidative polymerization of m-ABSA at anode potential. Meanwhile, a simple and sensitive sensor was fabricated to detect normetanephrine (NMN), which is one of the significant diagnostic markers for diseases. Compared with bare GCE, the p-m-ABSA film prepared on GCE surface has the advantage of increasing electrode surface area and active sites distinctly, thus obviously improving the electrocatalytic activity. The results demonstrated that the developed electrochemical sensor exhibited high sensitivity, stability, selectivity and excellent electrocatalytic activity towards NMN. The surface morphology of p-m-ABSA/GCE was characterized by scanning electron microscopy (SEM), indicating that the electrode surface had a layered structure. The preparation conditions and analysis methods of sensors were studied in detail. Under optimum conditions, peak current and concentrations of NMN were linearly related well from 0.5 to 30.0 µM with a limit of detection (S/N = =3) of 0.17 µM. Moreover, this modified sensor has also been successfully used for the detection of NMN in human serum samples.
研究领域:
生物医学工程
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分析化学
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DOI
高影响因子
Materials Today Bio
·
2026
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IF 11
Yujun Zhang,Fengfei Zhao,Feiyi Sun,Haiyan Chen,Lingling Wang,Rendy Hosea,Zheng Zhao,Ben Zhong Tang,Fei Sun,Xinghua Yu
The emergence of aggregation-induced emission (AIE) luminogens has revolutionized biomedical theranostics, yet the exploration of natural AIE-active therapeutics remains nascent. Herein, we propose a novel “AIE-Pharmacology” paradigm, employing the natural flavonoid acacetin as an intrinsic AIEgen with pharmacological activity for self-monitored therapy of asthenozoospermia. Overcoming traditional aggregation-caused quenching (ACQ), acacetin utilizes its aggregation-enhanced emission and excited-state intramolecular proton transfer (ESIPT) properties to enable simultaneous treatment, high-contrast imaging, and tracking. We developed an extracellular vesicles (EVs)-based co-delivery system loaded with acacetin and β-Nicotinamide mononucleotide (NMN). This nanoplatform (EVs@N + A) exhibits inherent affinity for the testicular microenvironment. Upon targeted accumulation, released acacetin triggers a potent anti-ferroptotic response by upregulating GPX4 and SLC7A11 and suppressing lipid peroxidation. In parallel, NMN elevates intracellular NAD + levels, reprogramming cellular metabolism and restoring ATP production. This dual strategy—inhibiting ferroptosis and rejuvenating metabolism—effectively rescues sperm function, enhancing sperm count, motility, and progressive movement in vivo . Our work reports acacetin as a multifunctional AIEgen in reproductive medicine and establishes a traceable theranostic platform, introducing the “AIE-Pharmacology” paradigm as a promising approach for treating male infertility and other diseases.
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DOI
PubMed
高影响因子
Journal of Ovarian Research
·
2026
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IF 5.3
Wang Yunduan,Li Qiao,Li Yueyue,Ma Zifeng,Xu Hongmei,Chen Kechao,Li Jian,Lan Daoliang,Fu Wei
Oxidative stress is a major driver of granulosa cell (GC) dysfunction and disrupted steroidogenesis. However, the mechanisms underlying oxidative stress–induced progesterone synthesis impairment and potential intervention strategies remain inadequately defined. In this study, RNA-seq re-analysis revealed that hydrogen peroxide (H₂O₂) markedly altered gene expression in mouse granulosa cells (mGCs), particularly affecting pathways related to progesterone biosynthesis. In vitro experiments confirmed that H₂O₂ suppresses progesterone production via downregulation of Sirtuin 1 (SIRT1). Conversely, β-nicotinamide mononucleotide (NMN) supplementation increased intracellular NAD⁺ levels, and upregulated SIRT1 and Nicotinamide phosphoribosyl transferase (NAMPT) expression. This regulation enhanced cell proliferation, stimulated the expression of progesterone biosynthetic enzymes, and promoted NAMPT transcriptional activity. Notably, the beneficial effects of NMN were diminished upon SIRT1 inhibition. Similarly, inhibition of NAMPT attenuated the positive regulatory effect of NMN, leading to a marked reduction in SIRT1 levels and a consequent suppression of progesterone secretion. Thus, SIRT1 activation induces NAMPT expression, which in turn feeds back to enhance SIRT1 activity and support progesterone biosynthesis. Together, these findings suggest that NMN alleviates H₂O₂-induced progesterone synthesis disruption in mGCs through activation of the NAD⁺/SIRT1/NAMPT axis, providing a potential therapeutic strategy for oxidative stress–related reproductive dysfunction.
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PubMed
高影响因子
Cellular and Molecular Gastroenterology and Hepatology
·
2024
·
IF 7.1
Liang Wang,Jinsong Li,Mingshan Jiang,Yue Luo,Xiaoke Xu,Juan Li,Yang Pan,Hu Zhang,Zhi-Xiong Jim Xiao,Yang Wang
Background and Aims Dysfunction of the intestinal epithelial barrier comprising the junctional complex of tight junctions and adherent junctions leads to increased intestinal permeability, which is a major cause of uncontrolled inflammation related to Inflammatory Bowel Disease (IBD). The NAD + -dependent deacetylase SIRT1 is implicated in inflammation and the pathological process of IBD. We aimed to elucidate the protective role and underlying mechanism of SIRT1 in cell-cell junction and intestinal epithelial integrity. Methods The correlation of SIRT1 expression and human IBD was analyzed by GEO or immunohistochemical analyses. BK5.mSIRT1 transgenic mice and WT mice were given dextran sodium sulfate (DSS) and the manifestation of colitis-related phenotypes were analyzed. Intestinal permeability was measured by FITC-Dextran and cytokines expression was analyzed by QPCR. The expression of the cell junction-related proteins in DSS-treated or SIRT1-knockdown Caco2 or HCT116 cells was analyzed by Western blotting. The effects of Nicotinamide mononucleotide (NMN) in DSS-induced mice colitis were investigated. Correlations of the SIRT1-β-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway with human IBD samples were analyzed. Results Reduced SIRT1 expression is associated with human IBD specimens. SIRT1 transgenic mice exhibit much-reduced manifestations of DSS-induced colitis. the activation of SIRT1 by NMN bolsters intestinal epithelial barrier function and ameliorates DSS-induced colitis in mice. Mechanistically, DSS down-regulates SiRT1 expression, leading to destabilization of β-TrCP1 and upregulation of Snail1, accompanied by reduced expression of E-cadherin, Occludin, and Claudin-1, consequently resulting in increased epithelial permeability and inflammation. The deregulated SIRT1-β-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway correlates with human IBD. Conclusion SIRT1 is pivotal in maintaining the intestinal epithelial barrier integrity via modulation of the β-TrCP1-Snail1-E-cadhein/Occludin/Claudin-1 pathway.
研究领域:
胃肠病学
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免疫学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
Food Quality and Safety
·
2026
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IF 4.9
Li Xiangyu,Liu Yingfei,Luo Yanbo,Jiang Xingyi,Chai Ying,Qiao Yuemei,Zhang Hongfei,Zhu Fengpeng,Pang Yongqiang,Chen Di
Nicotinamide mononucleotide (NMN) has gained significant attention as a promising anti-aging and health-promoting supplement, driving the development of efficient and sustainable production methods. Among these methods, enzymatic synthesis has emerged as a highly specific and environmentally friendly approach. This study presents a comprehensive evaluation of NMN synthesized via two key enzymatic pathways—nicotinamide riboside kinase (NRK)-mediated and nicotinamide phosphoribosyltransferase (NAMPT)-mediated routes—along with commercially available raw NMN materials. Key quality attributes, including purity, content, moisture levels, thermal stability, and biological activity, were systematically assessed. Results show that NAMPT-synthesized NMN consistently achieves 100% purity, matching pharmaceutical-grade standards, while NRK-synthesized NMN displays batch-dependent variability, with purity ranging from 92.13% to 96.19%. Stability analysis reveals that NAMPT-derived NMN maintains high thermal stability, whereas NRK-derived NMN undergoes significant physical and chemical degradation at elevated temperatures, with nicotinamide as the primary degradation product. Additionally, bioactivity testing demonstrated that NAMPT-derived NMN retains significantly higher biological activity compared with NRK-synthesized and commercial NMN. These findings provide essential data for optimizing NMN production processes and support the establishment of industry-wide quality control standards.
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高影响因子
Redox Biology
·
2024
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IF 10.7
Yue-Yue Guo,Nan-Nan Liang,Xiao-Yi Zhang,Ya-Hui Ren,Wen-Zheng Wu,Zhi-Bing Liu,Yi-Zhang He,Yi-Hao Zhang,Yi-Chao Huang,Tao Zhang,De-Xiang Xu,Shen Xu
Increasing evidences demonstrate that environmental stressors are important inducers of acute kidney injury (AKI). This study aimed to investigate the impact of exposure to Cd, an environmental stressor, on renal cell ferroptosis. Transcriptomics analyses showed that arachidonic acid (ARA) metabolic pathway was disrupted in Cd-exposed mouse kidneys. Targeted metabolomics showed that renal oxidized ARA metabolites were increased in Cd-exposed mice. Renal 4-HNE, MDA, and ACSL4, were upregulated in Cd-exposed mouse kidneys. Consistent with animal experiments, the in vitro experiments showed that mitochondrial oxidized lipids were elevated in Cd-exposed HK-2 cells. Ultrastructure showed mitochondrial membrane rupture in Cd-exposed mouse kidneys. Mitochondrial cristae were accordingly reduced in Cd-exposed mouse kidneys. Mitochondrial SIRT3, an NAD + -dependent deacetylase that regulates mitochondrial protein stability, was reduced in Cd-exposed mouse kidneys. Subsequently, mitochondrial GPX4 acetylation was elevated and mitochondrial GPX4 protein was reduced in Cd-exposed mouse kidneys. Interestingly, Cd-induced mitochondrial GPX4 acetylation and renal cell ferroptosis were exacerbated in Sirt3 −/− mice. Conversely, Cd-induced mitochondrial oxidized lipids were attenuated in nicotinamide mononucleotide (NMN)-pretreated HK-2 cells. Moreover, Cd-evoked mitochondrial GPX4 acetylation and renal cell ferroptosis were alleviated in NMN-pretreated mouse kidneys. These results suggest that mitochondrial GPX4 acetylation, probably caused by SIRT3 downregulation, is involved in Cd-evoked renal cell ferroptosis.
研究领域:
毒理学
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肾脏生理学
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细胞生物化学
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DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2023
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IF 4.3
Huiying Huang,Jian Shi,Zhongyi Li,Yifeng Rang,Weiye Li,Xueman Xiao,Congying Chen,Chunhong Liu
Nonylphenol (NP) exposure can trigger neurotoxicity and cause learning and memory impairment. Nicotinamide mononucleotide (NMN) has a therapeutic effect on neurodegenerative diseases , but the role of NMN on NP-induced learning and memory impairment is not known. Here, we examined the mitigative effect of NMN on the impaired learning and memory ability of rats exposed to NP. The NP impaired learning and memory in rats, while the low-dose intervention with NMN significantly prolonged the step-through latency of the PAT and improved the NAMPT and NMNAT1 content in brain tissue. At the same time, the NMN intervention also increased the content of 5-HTR 1A , 5-HTR 4 , and 5-HTR 6 related to learning and memory in the hippocampus. In line with this, we found that the NMN intervention activated the SIRT1/MAO-A pathway in brain tissue. NMN intervention, especially at 125 mg/kg doses, may improve rats’ NP-induced learning and memory impairment via the central 5-HT system and the NAD + /SIRT1/MAO-A pathway in the brain.
研究领域:
神经科学
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药理学
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毒理学
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产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
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2025
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IF 3.4
Ya-Xin Yao,Xue Lu,Zhao Li,Hao-Yu Liao,Zhi-Bing Liu,Hui Zhao,Hua Wang,De-Xiang Xu,Zhu-Xia Tan
Accumulating data demonstrate that bleomycin (BLM), a clinically used antineoplastic drug, induces pulmonary interstitial fibrosis. However, the specific mechanism remains unclear. This study was carried out for the purpose of evaluating the effect of mitochondrial dysfunction-associated senescence on BLM-induced pulmonary fibrosis. Adult C57BL/6 J mice were intratracheally instilled with BLM (2.5 mg/kg). Pulmonary α-SMA and Vimentin, two indicators of epithelial-mesenchymal transition (EMT), were increased, and pulmonary collagen deposition was shown in BLM-treated mice. Pulmonary p16 and p21, two biomarkers of cell cycle arrest, were elevated, and pulmonary SASP indicators were up-regulated in BLM-treated mice. The reduction of mitochondrial area in BLM-treated mouse lungs was revealed by transmission electron microscopy. ATP content was reduced in BLM-treated mouse lungs. Pulmonary SOD2 and IDH2, two enzymes located in mitochondria, were decreased in BLM-treated mice. Sirtuin3 (SIRT3), an NAD + -dependent deacetylase located in mitochondria, was down-regulated in BLM-treated mouse lungs. Interestingly, Sirt3 gene knockout aggravated BLM-evoked mitochondrial dysfunction-associated senescence in mouse lungs. Sirt3 gene knockout exacerbated BLM-induced lung fibrosis. Conversely, nicotinamide mononucleotide (NMN), an NAD + precursor, weakened BLM-induced down-regulation of mitochondrial SIRT3 activity in mouse lungs. NMN pretreatment attenuated BLM-induced mitochondrial dysfunction-associated senescence in mouse lungs. Finally, NMN pretreatment alleviated BLM-induced EMT and lung fibrosis. These results indicate that mitochondrial dysfunction-associated senescence partially contributed to BLM-induced pulmonary fibrosis.
研究领域:
分子生物学
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细胞生物学
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呼吸病学
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药理学
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遗传学
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生物化学
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DOI
PubMed
高影响因子
ADVANCED MATERIALS
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2023
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IF 29.4
Ruixue Duan,Yueping Li,Ruru Zhang,Xuelan Hu,Yi wang,Jianfeng Zeng,Mingyuan Gao
Acute kidney injury (AKI) induced by ischemia reperfusion is closely related to mitochondrial dysfunction. Nicotinamide adenine dinucleotide (NAD + ) can enhance the mitochondrial function and restrain the following inflammation, but it is hardly delivered and lacks renal targeting ability. To address these problems, we herein use an ultra-small Fe 3 O 4 nanoparticle as a carrier to deliver nicotinamide mononucleotide (NMN), a precursor of NAD + . An outstanding sophistication of the current design is that once NMN is attached on the surface of Fe 3 O 4 nanoparticles through its phosphate group, the remaining part is structurally highly similar to nicotinamide riboside, which provides an opportunity to deliver the NAD + precursor into renal cells through nicotinamide riboside kinase 1 on cell membrane. It was demonstrated that NMN-loaded Fe 3 O 4 nanoparticles can effectively reverse AKI induced by ischemia reperfusion. In-depth studies indicated that a well-timed iron replenishment following anti-inflammation treatment plays a determined role in recovering AKI, which distinguishes the current study from previously strategies centering on anti-ROS (reactive oxygen species), anti-inflammation or even iron elimination. This article is protected by copyright. All rights reserved
研究领域:
肾病学
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药学
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纳米技术
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分子生物学
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DOI
PubMed
高影响因子
Nature Communications
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2022
·Vol. 13
·期 1
·1-15
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IF 17.694
Hou Yun Nan,Cai Yang,Li Wan Hua,He Wei Ming,Zhao Zhi Ying,Zhu Wen Jie,Wang Qiang,Mai Xinyi,Liu Jun,Lee Hon Cheung,Stjepanovic Goran,Zhang Hongmin,Zhao Yong Juan
Sterile alpha (SAM) and Toll/interleukin-1 receptor (TIR) motif containing 1 (SARM1) is an autoinhibitory NAD-consuming enzyme that is activated by the accumulation of nicotinamide mononucleotide (NMN) during axonal injury. Its activation mechanism is not fully understood. Here, we generate a nanobody, Nb-C6, that specifically recognizes NMN-activated SARM1. Nb-C6 stains only the activated SARM1 in cells stimulated with CZ-48, a permeant mimetic of NMN, and partially activates SARM1 in vitro and in cells. Cryo-EM of NMN/SARM1/Nb-C6 complex shows an octameric structure with ARM domains bending significantly inward and swinging out together with TIR domains. Nb-C6 binds to SAM domain of the activated SARM1 and stabilized its ARM domain. Mass spectrometry analyses indicate that the activated SARM1 in solution is highly dynamic and that the neighboring TIRs form transient dimers via the surface close to one BB loop. We show that Nb-C6 is a valuable tool for studies of SARM1 activation.
研究领域:
分子生物学
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神经科学
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结构生物学
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细胞生物学
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DOI
PubMed
高影响因子
Advanced Science
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2025
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IF 14.1
Shuoting Zhou,Xi Xiong,Jialong Hou,Qi Duan,Yi Zheng,Tao Jiang,Jiani Huang,Haijun He,Jiaxue Xu,Keke Chen,Wenwen Wang,Jinlai Cai,Jingjing Qian,Huijun Chen,Weihong Song,XinShi Wang,Chenglong Xie
Serving as a pivotal hub for cellular metabolism and intracellular signaling, the mitochondrion has emerged as a crucial organelle whose dysfunction is linked to many human diseases, including neurodegenerative disorders, particularly Parkinson's disease (PD). However, whether mitochondrial quality control (MQC) can be targeted for therapeutic interventions remains uncertain. This study uses clinical samples, molecular biology techniques, pharmacological interventions, and genetic approaches to investigate the significance of NAD+ levels in cross-species models of PD. These results reveal that treatment of rotenone-incubated cells with NAD+ boosters (such as NMN, siCD38, and NAT) increases UPR mt /mitophagy-related MQC, reduces pro-inflammatory cytokine expression, inhibits apoptosis, and strengthen redox reactions. In vivo, NMN supplementation inhibits motor deficit and forestalls the neuropathological phenotypes of MPTP-induced PD mice, which are required for the atf4-related mitochondrial UPR pathway. Notably, bulk omics signatures and metabolomic profiling analyses of the striatum reveal NMN-induced transcriptional changes in genes and proteins involved in mitochondrial homeostasis. Thus, these findings demonstrate that the accelerated pathology in PD models is probably mediated by impaired MQC and that bolstering cellular NAD+ levels alleviates mitochondrial proteotoxic stress and mitigate PD phenotypes.
研究领域:
神经科学
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细胞生物学
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药理学
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分子生物学
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生物化学
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基因组学
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代谢组学
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产品关联
DOI
PubMed
高影响因子
ADVANCED FUNCTIONAL MATERIALS
·
2025
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IF 19
Shiyao Guo,Mingyue Zhang,Ke Zhang,Xiaotong Lu,Peiran Chen,Bangliu Yang,Xueqian Wang,Yuhong Zhuo,Dongqin Yu,Chao Qi,Kaiyong Cai
Osteoporosis compromises bone repair by generating a dysregulated microenvironment marked by excessive accumulation of reactive oxygen species (ROS) and a reduced pH. This pathological state leads to mitochondrial dysfunction, impaired osteogenic differentiation, and excessive activation of osteoclasts. In this study, a ROS-responsive titanium implant coating composed of calcium carbonate-mineralized nicotinamide mononucleotide (NMN) nanoparticles, lipoic acid-modified gelatin (LAMG), and sodium alginate (SA) is developed, designed to enhance osseointegration through dual synergistic mechanisms. First, the LAMG hydrogel effectively scavenges excess ROS, while calcium carbonate neutralizes H + ions and restores physiological pH levels, thereby reducing acid-induced bone resorption and inhibiting osteoclast activity. Second, ROS and H + ions-triggered release of NMN enhances the intracellular NAD⁺/NADH ratio in bone marrow mesenchymal stem cells, activates the SIRT1 signaling pathway, restores mitochondrial function, and promotes osteogenic differentiation. By concurrently remodeling the pathological bone microenvironment and repairing mitochondrial dysfunction, this multifunctional coating suppresses osteoclast-mediated bone resorption while facilitating osteoblast formation, thereby enhancing peri-implant osseointegration under osteoporotic conditions. This strategy not only presents a promising therapeutic approach for functionalizing titanium implants but also offers a potentially translatable platform for treating osteoporotic bone defects.
研究领域:
生物材料
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组织工程
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骨科
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再生医学
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纳米医学
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骨骼生物学
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生物医学工程
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产品关联
DOI
高影响因子
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