Journal of Fungi
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2025
·Vol. 11
·期 7
·513
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IF 4
Tengyu Ma,Hongguang Zhu,Jiajia Yin,Yu Tian,Wenjing Yan,Haixin Sun
Saccharomyces cerevisiaeoften undergoes strain degeneration during industrial serial subculturing, though this phenomenon remains understudied. This study first conducted strain screening and biological characterization through TTC (2,3,5-triphenyltetrazolium chloride) colorimetric assays, Durham tube fermentation gas production tests, and WL medium (Wallerstein Laboratory medium) cultivation. Subsequently, the changes in intergenerational biological traits after serial subculturing were investigated. Finally, transcriptomic analysis was employed to examine differential gene expression under high-glucose stress during continuous subculturing. The experimental results demonstrated that: (1) TheS. cerevisiaeQDSK310-Z-07 (GenBank: PP663884), isolated from farm soil, exhibited robust growth within a temperature range of 24–36 °C, with optimal growth observed at 28 °C. It thrived in a pH range of 4–5.5 and efficiently utilized various carbon and nitrogen sources; (2) After serial subculturing, the strain’s ethanol production capacity and fermentation rate partially declined and then stabilized, while maintaining strong tolerance to high ethanol concentrations and hyperosmotic stress; (3) Transcriptomic analysis revealed significant differential expression of genes related to lipid metabolism, amino acid metabolism, and other pathways under high-glucose stress following continuous subculturing. These findings elucidate the biological trait variations inS. cerevisiaeduring serial subculturing and provide key metabolic regulation candidate targets for its long-term adaptive evolution under high-glucose stress.
研究领域:
微生物学
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分子生物学
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生物技术
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PubMed
高影响因子
Oxidative Medicine and Cellular Longevity
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2022
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IF 7.31
Lili Shi,Yuliang Li,Meixin Shi,Xiaoxue Li,Guopeng Li,Jie Cen,Dan Liu,Can Wei,Yan Lin
Background. It is well-known that dysfunctions of vascular smooth muscle cells (VSMCs) act an essential part in vascular complications of diabetes. Studies have shown that circular RNAs (circRNAs) and microRNAs (miRNAs) play a crucial role in regulating cell functions. However, their influence on the proliferation, calcification, and autophagy of VSMCs remains to be further explored. Therefore, this study elucidates the role and mechanism of hsa_circRNA_0008028 in high glucose- (HG-, 30 mM) treated VSMCs in vitro. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was chosen to detect the levels of hsa_circRNA_0008028, miR-182-5p, and tribble 3 (TRIB3). Then, dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to predict and verify the binding relationship between miR-182-5p and hsa_circRNA_0008028 or TRIB3. Cell counting kit-8 assay, 5-ethynyl-2-deoxyuridine (EdU) staining, corresponding commercial kits, and western blotting were used to measure indexes reflecting cell viability, proliferation, calcification, and autophagy of VSMCs, respectively. Results. In HG-induced VSMCs, hsa_circRNA_0008028 and TRIB3 were highly expressed, whereas miR-182-5p decreased. Meanwhile, cell proliferation, calcification, and autophagy could be repressed by silencing of hsa_circRNA_0008028. However, these effects can be eliminated by miR-182-5p inhibition. Furthermore, it was demonstrated that hsa_circRNA_0008028 could promote the expression of TRIB3, a target of miR-182-5p, by directly sponging miR-182-5p. The expression of TRIB3 was suppressed by hsa_circRNA_0008028 knockout, which was rescued by miR-182-5p inhibition. Conclusion. This study reveals that hsa_circRNA_0008028 can act as a sponge of miR-182-5p and promote HG-induced proliferation, calcification, and autophagy of VSMCs partly by regulating TRIB3.
研究领域:
分子生物学
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细胞生物学
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糖尿病研究
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PubMed
高影响因子
BIORESOURCE TECHNOLOGY
·
2023
·
IF 11.4
Hossain M. Zabed,Suely Akter,Mudasir A. Dar,Jamila A. Tuly,Mukesh Kumar Aswathi,Junhua Yun,Jia Li,Xianghui Qi
This study aimed to produce enhanced fermentable sugars from a novel stover system through the bioprocessing of its soluble sugars and insoluble carbohydrates. The pretreatment conditions were optimized for this high sugar-containing stover (HSS) to control inhibitor formation and obtain enhanced fermentable sugar concentrations. The optimum temperature, acid loading, and reaction time for the pretreatment were 155 °C, 0.5%, and 30 min, respectively, providing up to 97.15% sugar yield and 76.51 g/L total sugars at 10% solid-load. Sugar concentration further increased to 126.9 g/L at 20% solid-load, generating 3.89 g/L acetate, 0.92 g/L 5-hydroxymethyl furfural, 0.82 g/L furfural, and 3.75 g/L total phenolics as inhibitors. To determine the effects of soluble sugars in HSS on fermentable sugar yield and inhibitor formation, sugar-removed HSS was further studied under the optimum conditions. Although prior removal of sugars exhibited a reduction in inhibitor generation, it also decreased total fermentable sugar production to 115.45 g/L.
研究领域:
生物技术
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可再生资源工程
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PubMed
高影响因子
Drug Design Development and Therapy
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2022
·
IF 4.319
Yu Li,Ximei Wang
Purpose High glucose environment in diabetes mellitus induces the dysfunction of bone marrow-derived mesenchymal stromal cells (BMSCs) and impairs bone regeneration. Chrysin is a natural polyphenol with outstanding anti-inflammation and anti-oxidation ability. However, whether and how chrysin affects BMSCs in high glucose conditions remain poorly understood. The present study aimed to explore the effects and underlying mechanisms of chrysin on the BMSCs exposed to high glucose environment.Materials and Methods Cell viability was detected by cell counting kit 8 assay and 5-ethynyl-2’-deoxyuridine staining, while cell apoptosis was determined through flow cytometry using Annexin V-FITC/PI kit. The oxidative stress in BMSCs was evaluated by detecting the reactive oxygen species production, malondialdehyde content, and superoxide dismutase activity. Alkaline phosphatase staining, Alizarin Red staining, and quantitative real-time PCR were performed to determine the osteogenic differentiation. Western blot was used to examine the expression of the PI3K/ATK/Nrf2 signaling pathway. Furthermore, chrysin was injected into calvarial defects of type 1 diabetic SD rats to assess its in vivo bone formation capability.Results Chrysin reduced oxidative stress, increased cell viability, and promoted osteogenic differentiation in BMSCs exposed to high glucose. Blocking PI3K/ATK/Nrf2 signaling pathway weakened the beneficial effects of chrysin, indicating that chrysin at least partly worked through the PI3K/ATK/Nrf2 pathway.Conclusion Chrysin can protect BMSCs from high glucose-induced oxidative stress via the activation of the PI3K/AKT/Nrf2 pathway, and promote bone regeneration in type 1 diabetic rats.
研究领域:
细胞生物学
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分子生物学
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糖尿病研究
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DOI
PubMed
高影响因子
Frontiers in Chemistry
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2024
·
IF 3.8
Xuyan Sun,Hua Yang,Han Zhang,Weiwei Zhang,Chunyu Liu,Xiaoxiao Wang,Wenping Song,Lin Wang,Qingsong Zhao
Dermal fibroblasts play a crucial role in the formation of granulation tissue in skin wounds. Consequently, the differentiation, migration, and proliferation of dermal fibroblasts are considered key factors in the skin wound healing process. However, in patients with diabetic foot ulcers, the proliferation and migration of fibroblasts are impaired by reactive oxygen species and inflammatory factors impair. Therefore, a novel magnetic gelatin-hesperidin microrobots drug delivery system was developed using microfluidics. The morphology, motility characteristics, and drug release of the microrobot were assessed, along with its impact on the proliferation and migration of human dermal fibroblasts under high-glucose conditions. Subjected to a rotating magnetic field, the microrobots exhibit precise, controllable, and flexible autonomous motion, achieving a maximum speed of 9.237 μm/s. In vitro drug release experiments revealed that approximately 78% of the drug was released within 30 min. It was demonstrated through cellular experiments that the proliferation of human dermal fibroblasts was actively promoted by the nanorobot, the migration ability of fibroblasts in a high-glucose state was enhanced, and good biocompatibility was exhibited. Hence, our study may provide a novel drug delivery system with significant potential for promoting the healing of diabetic foot wounds.
研究领域:
生物医学工程
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药学
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组织工程
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PubMed
高影响因子
Stem Cell Research & Therapy
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2025
·Vol. 16
·期 1
·1-21
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IF 7.3
Zhu Yanlin,Yang Yuhan,Lan Yuyan,Yang Zun,Gao Xiang,Zhou Jie
Background Diabetes mellitus (DM) and periodontitis have a bidirectional relationship, with each being a high-risk factor for the other. Prolonged hyperglycemia exacerbates periodontal inflammation and disrupts bone homeostasis. Pyruvate kinase M2 (PKM2), a key enzyme in glycolysis, is involved in metabolic reprogramming, but its role in osteogenesis under high-glucose (HG) inflammatory conditions remains largely unknown. This study aimed to investigate the effects of HG and inflammation on bone marrow mesenchymal stem cells (BMSCs) under indirect co-culture conditions and to explore how PKM2 regulates metabolism and mitochondrial function during osteogenic differentiation in HG inflammatory environments, elucidating its role in diabetic periodontitis (DP).Methods Expose BMSCs to conditioned medium (CM) collected from RAW264.7 cells stimulated with HG and/or lipopolysaccharide (LPS). BMSCs functionality was assessed using CCK8, EdU, Annexin V-PI apoptosis assay, alkaline phosphatase (ALP), and Alizarin Red S (ARS) staining. Metabolic characteristics were evaluated through Seahorse assays, lactate production, glucose uptake, and ATP measurements. Mitochondrial function was assessed via JC-1, and ROS staining, Mito-Tracker staining, and transmission electron microscopy (TEM). Gene and protein expression were analyzed by quantitative real-time PCR and western blotting. In vivo therapeutic effects of shikonin were validated via micro-CT and histological staining in a diabetic periodontitis mouse model.Results In vitro experiments demonstrated that HG inflammatory conditions impaired the survival of BMSCs, suppressed osteogenic differentiation, and induced metabolic reprogramming. This reprogramming was characterized by enhanced glycolysis, impaired oxidative phosphorylation (OXPHOS), abnormal upregulation of PKM2 expression, and mitochondrial dysfunction accompanied by morphological alterations. Shikonin effectively reversed these adverse effects by inhibiting PKM2 tetramerization, rescuing the loss of osteogenic function in BMSCs. The therapeutic potential of shikonin was confirmed in the diabetic periodontitis mouse model.Conclusion PKM2 impairs the osteogenesis of BMSCs by affecting metabolism and mitochondrial function, suggesting it as a potential therapeutic target for diabetic periodontitis.
研究领域:
细胞生物学
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代谢组学
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口腔医学
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DOI
PubMed
高影响因子
CELL BIOLOGY INTERNATIONAL
·
2022
·Vol. 46
·期 12
·2220-2231
·
IF 4.473
Maomao Miao,Yang Zhang,Xuping Wang,Shanshan Lei,Xiaowen Huang,Luping Qin,Dan Shou
Diabetic osteoporosis (DOP) is a disorder of bone metabolism induced by multiple mechanisms. Previous studies have revealed that microRNAs (miRNAs) play crucial roles in bone metabolism. MiRNA-144-5p has been proven to participate in the regulation of osteoblast activities; however, its specific mechanism in DOP has not been elucidated. This study investigated whether high glucose (HG) inhibited osteoblasts by regulating miRNA-144-5p. Our results showed that HG inhibited bone formation not only in vivo but also in vitro. We observed that HG severely hindered the migration, proliferation and mineralization of osteoblasts, while miRNA-144-5p was upregulated by way of the cell counting kit-8 assay, wound healing assay, alkaline phosphatase (ALP) activity assay and alizarin red staining. Double luciferase reporter experiments showed that miRNA-144-5p directly targeted insulin receptor substrate 1 (IRS1). The IRS1/AKT signaling pathway is closely related to osteoblasts' migration, proliferation, and mineralization. Silencing miRNA-144-5p promoted the mRNA, and protein expression of IRS1, thereby letting the expression of total AKT down, and then preventing phosphorylation of AKT into the nucleus to regulate migration, proliferation, and mineralization genes of osteoblasts. In conclusion, this study indicated that HG regulated the migration, proliferation, and mineralization of osteoblasts via the miRNA-144-5p/IRS1/AKT axis, which suggested a possible mechanism for DOP pathology.
研究领域:
分子生物学
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内分泌学
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骨代谢
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糖尿病
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DOI
PubMed
高影响因子
Journal of Translational Medicine
·
2025
·Vol. 23
·期 1
·1-19
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IF 7.5
Han Ning,Yu Na,Yu Li
Background Diabetic retinopathy (DR) is the common cause of diabetic vascular complications and it causes blindness. Until now, there are still some patients with DR who lack effective treatment. Tripartite motif containing 44 (TRIM44) has been shown to play a significant role in endothelial cells. However, the role of TRIM44 in DR remains unknown. Methods Diabetes was induced in rats through the administration of an intraperitoneal injection of 65 mg/kg of streptozotocin (STZ). Rat retinal microvascular endothelial cells (RMECs) were subjected to stimulation under high glucose (HG) conditions. A thorough proteomic investigation and bioinformatic analysis were performed to identify the differentially expressed proteins (DEPs) in rat RMECs after blocking TRIM44. A dual luciferase reporter assay was employed to assess the luciferase activity of TRIM44. Results TRIM44 was highly expressed in the retinal tissues of rats with diabetes and HG-induced RMECs. In vivo assays suggested that TRIM44 silencing improved the pathological alterations of DR rats as demonstrated by the downregulated expression of isolectin-B4 and VEGFA, along with a decrease in acellular capillaries within the retinal tissues. Knockdown of TRIM44 markedly reduced cell viability, proliferation, migration, invasion, and angiogenesis in HG-evoked RMECs. Mechanistically, TRIM44 was demonstrated to be activated transcriptionally by KLF transcription factor 9 (KLF9), a known facilitator of angiogenesis in DR. In HG-induced cells, the loss of TRIM44 resulted in the reverse of the endothelial cell function caused by KLF9 overexpression. After the comprehensive analysis, 64 upregulated and 38 downregulated DEPs were screened out for a series of functional enrichment analyses. Conclusions Collectively, this study demonstrates that TRIM44 knockdown suppressed diabetes-induced retinal vascular dysfunction in DR.
研究领域:
分子生物学
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糖尿病学
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眼科学
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DOI
PubMed
高影响因子
Molecular Medicine Reports
·
2023
·Vol. 27
·期 2
·1-10
·
IF 3.4
Cunyang Gu,Feng Gao,Shiqi Zhang,Lihua Kang,Wei Zhang,Xiaojuan Feng,Jinxi Liu,Yuexin Tian,Qun Wei,Yunxia Du,Yujia Xing,Qingjuan Liu,Shuxia Liu
Tubulointerstitial fibrosis (TIF) is an important pathological change that occurs during the development of diabetic kidney disease. The epithelial‑mesenchymal transition (EMT) of renal tubular epithelial cells is a manifestation of TIF. STAT1, a member of the STAT family of transcription factors, can be modified by the small ubiquitin‑related modifier (SUMO), thus affecting the activity of STAT1. The present study investigated the role of STAT1 SUMOylation in high glucose‑induced tubular EMT by western blotting, immunocytochemistry, immunofluorescence, co‑immunoprecipitation and dual luciferase reporter analysis. The results indicated that in the process of high glucose‑induced EMT, STAT1 activation protected the cells from EMT. However, high glucose also increased the SUMOylation of STAT1, which prevented STAT1 from exerting an effective protective role by inhibiting its activity.
研究领域:
分子生物学
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细胞生物学
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糖尿病研究
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肾病学
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DOI
PubMed
高影响因子
PeerJ
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2023
·
IF 2.7
Linlin Sun,Miao Ding,Fuhua Chen,Dingyu Zhu,Xinmiao Xie
Podocyte injury is a critical factor in the pathogenesis of diabeticnephropathy (DN). Emerging evidence has demonstrated that breviscapine (Bre) exerts a renoprotective effect on diabetic rats. However, the effects of Bre on regulating podocyte injury under high glucose (HG) conditions remain unclear. In this study, an experimental mouse model of DN was induced by intraperitoneal injections of streptozotocin (STZ) in vivo . The effects of Bre on podocyte injury were assessed using cell counting kit-8 (CCK-8) assay, TdT-mediated dUTPnick-endlabelling (TUNEL) staining, quantitative real-time PCR (qRT‒PCR) and western blot analysis. We found that renal function was significantly decreased in diabetic mice, and this effect was blocked by Bre treatment. Bre effectively increased podocyte viability and inhibited HG-induced cell apoptosis. Furthermore, Bre ameliorated HG-induced podocyte injury, as evidenced by decreased α-smooth muscle actin (α-SMA) expression and increased podocin and synaptopodin expression. Mechanistically, Bre inhibited HG-induced nuclear factorkappaB (NF-κB) signalling activation and subsequently decreased NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, resulting in a decrease in pyroptosis. Pharmacological inhibition of NLRP3 decreased HG-induced podocyte injury, whereas the NLRP3 agonist abrogated the effects of Bre on inhibiting podocyte injury. In summary, these results demonstrate that Bre alleviates HG-induced podocyte injury and improves renal function in diabetic mice, at least in part by inhibiting NF-κB/NLRP3-mediated pyroptosis.
研究领域:
药理学
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肾病学
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分子生物学
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PubMed
高影响因子
BIOGERONTOLOGY
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2024
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IF 4.4
Yuan Qianhua,Luo Mengliu,Xie Yutong,Song Wanhan,Wang Ya,Deng Dazhang,Chen Shuyan,Guo Honghui
Aging entails the progressive decline in the body’s self-regulation and functionality over time. Notably, obesity and aging exhibit parallel phenotypes, with obesity further accelerating the aging process across multiple dimensions and diminishing lifespan. In this study, we explored the impact of trans fatty acid (TFA) consumption on the overall health and lifespan of male Drosophila melanogaster under an isocaloric high-sugar and high-fat diet. Our results indicate that TFA intake results in a shortened lifespan, elevated body weight, and increased triglyceride levels in flies fed a high-sugar and high-fat diet with equivalent caloric intake. Additionally, TFA exposure induces oxidative stress, locomotor deficits, and damage to the intestinal barrier in flies. Collectively, chronic TFA consumption expedites the aging process and reduces the lifespan of male Drosophila melanogaster . These results contribute supplementary evidence regarding the adverse health effects associated with TFAs. Graphical Abstract Trans fatty acid intake results in a shortened lifespan, elevated body weight, and increased triglyceride levels in male Drosophila melanogaster fed a high-sugar and high-fat diet with equivalent caloric intake. Additionally, Trans fatty acid exposure induces oxidative stress, locomotor deficits, and damage to the intestinal barrier in flies.
研究领域:
营养学
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衰老
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代谢
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果蝇遗传学
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PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 7
·3048
·
IF 4.9
Aimin Qiao,Meiqing Pan,Yue Zeng,Ying Gong,Yunfeng Zhang,Xiucai Lan,Lei Tang,Weizhang Jia
Matrine, a quinoline alkaloid, possesses lipid-regulating effects, but the underlying mechanisms are rarely characterized in vivo. With a fat-accumulating Caenorhabditis elegans model, we show that matrine reduces the fat content and the DHS-3::GFP-labeled lipid droplets in high-glucose-diet N2 and transgenic LIU1 nematodes, respectively. Based on RNA-seq, this study demonstrates that a loss of AAK-2 function suppresses the fat-lowering effects of matrine, and the hyperactivated AAK-2 strain has a relatively lower fat content than N2. The involvement of NHR-49 in matrine’s fat-lowering effects further suggests that matrine impacts fat breakdown and storage via the AAK-2/NHR-49-governed pathway. Using the transgenic SJ4143 ( ges-1::GFP(mit) ) and VS10 ( vha-6p::mRFP-PTS1 ), we show that matrine activates the AAK-2/NHR-49 pathway, coupling the alteration of mitochondrial and peroxisomal functions. Studies of aak-2 and nhr-49 mutants reveal that AAK-2 and NHR-49 modulate lipid metabolic homeostasis; meanwhile, matrine increases physical fitness and lifespan through activating the AAK-2/NHR-49 pathway in high-glucose-diet nematodes. Surprisingly, we found that β-amyloid (Aβ) induces lipid metabolic disorder in an Alzheimer’s disease (AD) C. elegans model, but matrine not only reduces Aβ aggregation but also alleviates Aβ-mediated lipid metabolic disorder. Our data suggest that matrine has promise as a fat-lowering agent, and also offer new insights into its therapeutic potential for AD.
研究领域:
生物化学
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分子生物学
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药理学
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DOI
PubMed
高影响因子