BIOLOGICAL TRACE ELEMENT RESEARCH
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2024
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IF 3.4
Zhu Jiamei,Nie Gaohui,Dai Xueyan,Wang Dianyun,Li ShanXin,Zhang Caiying
Cadmium (Cd) and high molybdenum (Mo) pose deleterious effects on health. Prior studies have indicated that exposure to Mo and Cd leads to damage in duck kidneys, but limited studies have explored this damage from the perspective of fatty acid metabolism. In this study, 40 healthy 8-day-old ducks were randomly assigned to four groups and fed a basic diet containing Cd (4 mg/kg Cd) or Mo (100 mg/kg Mo) or both. Kidney tissues were harvested on the 16th week. Results demonstrated that Cd and/or Mo inhibited mitochondrial fatty acid β-oxidation and disrupted mitochondrial dynamics, along with significant suppression of peroxisome proliferator-activated receptor β/δ (PPARβ/δ) protein in duck kidneys. In vitro study, duck renal tubular epithelial cells were exposed for 12 h to either Mo (480 μM Mo), Cd (2.5 μM Cd), and GW0742 (0.3 μM, a potent agonist of PPARβ/δ) alone or in combination. The results demonstrated that Cd and/or Mo led to marked fatty acid oxidation deficiency and mitochondrial dysfunction and that PPARβ/δ protein was involved in the process. Altogether, this study found that activating PPARβ/δ-mediated fatty acid β-oxidation mitigates mitochondrial dysfunction co-induced by Mo and Cd in duck kidneys.
研究领域:
毒理学
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分子生物学
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PubMed
高影响因子
Drug Design Development and Therapy
·
2024
·
IF 4.7
Chaoying Jin,Ruolin Zhao,Weihang Hu,Xiaolong Wu,Li Zhou,Letian Shan,Huiling Wu
Background Pressure ulcer is common in the bedridden elderly with high mortality and lack of effective treatment. In this study, human-adipose-derived-stem-cells-hyaluronic acid gel (hADSCs-HA gel) was developed and applied topically to treat pressure ulcers, of which efficacy and paracrine mechanisms were investigated through in vivo and in vitro experiments.Methods Pressure ulcers were established on the backs of C57BL/6 mice and treated topically with hADSCs-HA gel, hADSCs, hyaluronic acid, and normal saline respectively. The rate of wound closure was observed continuously during the following 14 days and the wound samples were obtained for Western blot, histopathology, immunohistochemistry, and proteomic analysis. Human dermal fibroblasts (HDFs) and human venous endothelial cells (HUVECs) under normal or hypoxic conditions were treated with conditioned medium of human ADSCs (ADSC-CM), then CCK-8, scratch test, tube formation, and Western blot were conducted to evaluate the paracrine effects of hADSCs and to explore the underlying mechanism.Results The in vivo data demonstrated that hADSCs-HA gel significantly accelerated the healing of pressure ulcers by enhancing collagen expression, angiogenesis, and skin proliferation. The in vitro data revealed that hADSCs strengthened the proliferation and wound healing capabilities of HDFs and HUVECs, meanwhile promoted collagen secretion and tube formation through paracrine mode. ADSC-CM was also proved to exert protective effects on hypoxic HDFs and HUVECs. Besides, the results of proteomic analysis and Western blot elucidated that lipid metabolism and PPARβ/δ pathway mediated the healing effect of hADSCs-HA gel on pressure ulcers.Conclusion Our research showed that topical application of hADSCs-HA gel played an important role in dermal regeneration and angiogenesis. Therefore, hADSCs-HA gel exhibited the potential as a novel stem-cell-based therapeutic strategy of treating pressure ulcers in clinical practices.
研究领域:
生物医学工程
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干细胞生物学
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组织工程
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伤口愈合
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PubMed
高影响因子
npj Science of Food
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2025
·Vol. 9
·期 1
·1-9
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IF 7.8
Ye Xiang,Chen Wen,Yan Fujie,Zheng Xiaodong,Tu Pengcheng
In late-stage type 2 diabetes mellitus (T2DM), impaired islet β cell function leads to absolute insulin deficiency, thereby disrupting blood glucose homeostasis. GLP-1, an incretin hormone, stimulates insulin secretion from islet β cells post-meals. This study investigated the effects of anthocyanin cyanidin-3-O-glucoside (C3G) on GLP-1 secretion using STC-1 (intestinal endocrine L cells) and NIT-1 (islet β cells). In a co-culture system, C3G treatment increased GLP-1 secretion in STC-1 cells, promoting insulin release in NIT-1 cells under high glucose. Mechanistically, C3G activated the PPARβ/δ-β-catenin-TCF-4 pathway in STC-1 cells, enhancing PG precursor transcription and GLP-1 synthesis.Inhibiting PPARβ/δ with GSK0660 blocked this C3G-induced upregulation. Overall, C3G stimulates GLP-1 secretion from intestinal L cells via this pathway, indirectly boosting insulin release from β cells. These findings enhance T2DM mechanism understanding and suggest the potential of C3G in GLP-1-based T2DM therapy.
研究领域:
分子生物学
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代谢疾病研究
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药理学
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POULTRY SCIENCE
·
2025
·
IF 4.2
Shanxin Li,Gaohui Nie,Xueyan Dai,Jiamei Zhu,Li Xiao,Sunan Wang,Jirong Chen,Jianrong Ren,Caiying Zhang
Excessive molybdenum (Mo) and cadmium (Cd) exert negative influences on organism. Our prior experiments attested that Mo and Cd brought liver damage in ShaoXing ducks ( Anas platyrhyncha ); this injury mechanism has not yet been fully clarified. Hence, the hepatotoxicity mechanisms of Mo and Cd were roundly analyzed by network toxicology in the study, the analysis confirmed that Mo and Cd primarily induce liver injury through lipid metabolism dysregulation, oxidative stress, and mitochondrial dysfunction. Further validation demonstrated that Mo and/or Cd upregulated fatty acid synthesis, reduced PPARβ/δ-mediated fatty acid β-oxidation, promoted free fatty acids (FFA) content and mitochondrial reactive oxygen species (mtROS) level, impaired integrality of mitochondrial membrane and mitochondrial function, thereby causing fatty acid metabolism disarray and mitochondrial dysfunction. Both PPARβ/δ activator GW0742 and mtROS inhibitor ROS-IN-1 could alleviate the changes of above these indexes. Collectively, findings from this research showed that Cd and Mo additively caused crosstalk between fatty acid metabolism disarray and mitochondrial dysfunction, thus inducing liver injury in ducks.
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Cells
·
2025
·Vol. 14
·期 23
·1843
·
IF 5.2
Shijie Li,Yan Cui,Xinrui Li,Xuefeng Bai,Denghui Wang,Pengfei Zhao,Pengqiang Wei,Sijiu Yu,Junfeng He
Background: In the cold plateau environment, the yak’s coat exhibits significant adaptive regulation to cope with adverse conditions. This adaptation is fundamentally governed by the cycle of hair follicles (HFs), a complex process involving numerous molecular signals. However, the key regulators and underlying pathways remain poorly understood. Methods: Proteomic and non-targeted metabolomic analyses were employed to systematically investigate changes in proteins and metabolites during the cycle of yak hair follicles. We further validated the expression dynamics of PPARβ/δ and its related molecules, as well as the specific biological role of PPARβ/δ in regulating lipid metabolism and influencing the proliferation and apoptosis of yak dermal papilla cells (DPCs). Results: Proteomic results indicated that lipid-related proteins were among the most significantly altered, second only to hair structural proteins. The PPAR signaling pathway, which regulates lipid metabolism, may also play an important role in the cycle of yak HF. Non-targeted metabolomics revealed that Fatty Acyls were the most significantly altered metabolites during the transitions into anagen and catagen. Notably, unsaturated long-chain fatty acids (PPARβ/δ agonists) were consistently up-regulated in anagen and down-regulated in catagen, whereas saturated long-chain fatty acids (lacking PPARβ/δ agonist activity) did not exhibit a similar trend. PPARβ/δ shows significant expression changes in the dermal papilla (DP) and hair matrix (HM) during the cycle of yak HFs. Specifically, PPARβ/δ expression in the DP underwent progressive downregulation during the transition from anagen to catagen and subsequently to telogen, becoming nearly undetectable in the telogen DP. Cellular experiments confirmed that PPARβ/δ activation significantly reduced intracellular lipid content in yak DPCs and was accompanied by increased proliferation. Conversely, PPARβ/δ inhibition led to intracellular lipid accumulation and decreased proliferation. Conclusions: These findings suggest that PPARβ/δ may regulate the yak HF cycle by modulating lipid metabolism in DP. The level of intrinsic lipid metabolism within HFs may be a key factor influencing yak HF growth.
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