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Simvastatin mitigates vascular cognitive impairment in rat’s hippocampus in lacunar cerebral infarction 辛伐他汀减轻腔隙性脑梗死大鼠海马的血管性认知障碍
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2024-01-01 DOI: 10.1166/mex.2024.2612
Sihan Chen, Yening Zhu, Zhuqin Li, Donger Chen
Simvastatin is used to treat Alzheimer’s disease with impaired cognitive function through blocking of PI3K/Akt signaling to inhibit survival of new neurons and growth of neurons. This study investigated the potential of simvastatin on vascular cognitive impairment (VCI) caused by lacunar cerebral infarction (LCI) in the hippocampus of rats. After establishment of LCI models, rats were administered with NaOH solution (model group), simvastatin (simvastatin group), and PI3K/Akt pathway inhibitor (inhibitor group), respectively, and 10 healthy rats served as control group. Upon treatment, Y-maze and Morris water maze detected spatial cognition ability of rats; while cleaved caspase-3 staining was used to assess apoptosis in the hippocampus. Western blot analysis detected Akt and ERK1/2 phosphorylation levels and enzyme-linked immuno sorbent assay (ELISA) determined the content of brain-derived neurotrophic factor (BDNF). The Y maze Morris water maze confirmed impairment of long-term memory abilities in the LCI rats from the model group. Treatment with simvastatin significantly improved correct rate of arm alternates in rats and shorted the stage latency in the hidden platform experiment. The number of apoptotic cells increased in the hippocampal DG sub-granular area of rats with LCI, and BDNF level was significantly reduced. Administration of simvastatin suppressed cell apoptosis and increased BDNF level when improving phosphorylation level of Akt and ERK1/2 as well. Cerebral ischemia following LCI affects short and long-term memory, which leads to VCI. Simvastatin increases Akt and ERK1 in PI3K/Akt pathway, and hence up-regulates hippocampal BDNF levels, which promotes the regeneration of rat hippocampal nerve cells to relieve VCI.
辛伐他汀通过阻断PI3K/Akt信号传导,抑制新神经元的存活和生长,从而治疗认知功能受损的阿尔茨海默病。本研究探讨了辛伐他汀对大鼠海马腔隙性脑梗塞(LCI)引起的血管性认知障碍(VCI)的潜在影响。LCI模型建立后,分别给大鼠注射NaOH溶液(模型组)、辛伐他汀(辛伐他汀组)和PI3K/Akt通路抑制剂(抑制剂组),10只健康大鼠为对照组。治疗后,Y-迷宫和莫里斯水迷宫检测大鼠的空间认知能力;而裂解的caspase-3染色则用于评估海马的细胞凋亡。Western 印迹分析检测了 Akt 和 ERK1/2 磷酸化水平,酶联免疫吸附试验(ELISA)测定了脑源性神经营养因子(BDNF)的含量。Y迷宫莫里斯水迷宫证实了模型组LCI大鼠的长期记忆能力受损。辛伐他汀能显著提高大鼠手臂交替的正确率,并缩短隐藏平台实验中的阶段潜伏期。LCI大鼠海马DG粒下区凋亡细胞数量增加,BDNF水平明显降低。服用辛伐他汀可抑制细胞凋亡,提高BDNF水平,同时改善Akt和ERK1/2的磷酸化水平。LCI后的脑缺血会影响短期和长期记忆,从而导致VCI。辛伐他汀能增加PI3K/Akt通路中的Akt和ERK1,从而上调海马BDNF水平,促进大鼠海马神经细胞再生,缓解VCI。
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引用次数: 0
Effect of initial twins on mechanical properties of additive manufacturing CoCrNi alloy and molecular dynamic simulation 初始孪晶对增材制造 CoCrNi 合金机械性能的影响及分子动力学模拟
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2024-01-01 DOI: 10.1166/mex.2024.2593
Xu Kong, Haiyi Cheng, Yuying Jiang, Di Hu
The influence of twins on laser additive CoCrNi MEA was analyzed by experiments and molecular dynamic simulation. Results showed that the traditional laser additive CoCrNi MEA was prone to slip in the (111) direction. EBSD analysis showed an obvious 60°(111} axial angle pair relationship, which is related to the slower cooling rate. The results of molecular dynamic simulation showed that the yield strength of CoCrNi MEA increases first and then decreases, and the material has a critical twin density. When the twin density is less than the critical twin density, the strength of the material increases due to the thinning effect of the twin boundary on the grain. When the twin density is greater than the boundary twin density, the nucleation and proliferation of the twin boundary and the junction of the two become the dominant factors of the material deformation. When the twin density is far from the critical value, the twin spacing becomes smaller, the dislocation sources increase, the dislocation nucleation and proliferation increase, and the strength of the material decreases.
通过实验和分子动力学模拟分析了孪晶对激光添加剂钴铬镍 MEA 的影响。结果表明,传统的激光添加钴铬镍 MEA 在(111)方向上容易发生滑移。EBSD 分析显示出明显的 60°(111} 轴角对关系,这与冷却速度较慢有关。分子动力学模拟结果表明,钴铬镍 MEA 的屈服强度先增大后减小,材料具有临界孪晶密度。当孪晶密度小于临界孪晶密度时,由于孪晶边界对晶粒的减薄作用,材料的强度会增加。当孪晶密度大于边界孪晶密度时,孪晶边界的成核和增殖以及两者的交界成为材料变形的主导因素。 当孪晶密度远离临界值时,孪晶间距变小,位错源增加,位错成核和增殖增加,材料强度降低。
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引用次数: 0
Curcumin targets miR-1297 to promote mitochondrial apoptosis and cisplatin sensitization of lung cancer stem cells 姜黄素以 miR-1297 为靶标,促进线粒体凋亡和顺铂对肺癌干细胞的敏感性
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2024-01-01 DOI: 10.1166/mex.2024.2597
Jiayang Sun, Luzhi Gang, Chunlin Li
The medicinal value of curcumin has been confirmed in many diseases. This study explores miR-1297’s role in lung cancer cells. The targeting regulation between miR-1297 and BH3-only was analyzed by luciferase activity. Cisplatin (DDP)-resistant cell lines A549/DDP and NCI-H460/DDP were established followed by analysis of cell proliferation activity, BH3-only expression, and cell proliferation by EdU staining. miR-1297 targets BH3-only. miR-1297 expression in A549/DDP and NCI-H460/DDP cells was significantly increased while BH3-only was reduced. Same dose of DDP inhibited the proliferation of A549/DDP and NCI-H460/DDP cells. BH3-only in A549/DDP and NCI-H460/DDP cells in miR-1297 inhibitor transfection group was significantly increased, apoptosis was increased, proliferation was weakened, and drug resistance was reduced. Lung cancer DDP resistance is related to the expression of miR-1297. Down-regulation of miR-1297 can reduce the DDP drug resistance by increasing the expression of BH3-only.
姜黄素在许多疾病中的药用价值已得到证实。本研究探讨了 miR-1297 在肺癌细胞中的作用。研究通过荧光素酶活性分析了 miR-1297 与纯 BH3 之间的靶向调控。研究建立了耐顺铂(DDP)细胞系 A549/DDP 和 NCI-H460/DDP,然后用 EdU 染色法分析了细胞增殖活性、纯 BH3 表达和细胞增殖。相同剂量的 DDP 可抑制 A549/DDP 和 NCI-H460/DDP 细胞的增殖。miR-1297抑制剂转染组的A549/DDP和NCI-H460/DDP细胞中纯BH3明显增加,细胞凋亡增加,增殖减弱,耐药性降低。肺癌DDP耐药性与miR-1297的表达有关。下调miR-1297可以通过增加纯BH3的表达来降低DDP耐药性。
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引用次数: 0
Expression analysis of insulin-like growth factor 1, neutrophil/lymphocyte ratio, and inflammatory factors in children with Mycoplasmal pneumonia 支原体肺炎患儿胰岛素样生长因子 1、中性粒细胞/淋巴细胞比率和炎症因子的表达分析
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2572
Zhaoyan Wang, Xian Wang, Wanglan Zhao, Jun Luo
Mycoplasma pneumonia (MPP) belongs to atypical pneumonia, which is caused by Mycoplasma pneumonia infection, accounting for 10–40% of children’s community pneumonia. It is more common in children at preschool age. The clinical symptoms of MPP are varied and difficult to cure. The research analyze the expression of inflammatory factors in MPP, neutrophil/lymphocyte ratio (NLR), insulin-like growth factor 1 (IGF1). The aim is to provide relevant basis for treatment and diagnosis of the disease. 40 normal children were selected as the control group. 78 children with MPP were selected as the observation group. The levels of interleukin-6 (IL-6) and interleukin-2 (IL-2) in peripheral blood were detected. Platelet/lymphocyte ratio (PLR) and NLR were tested. IGF1 expression was determined by ELISA. The correlation between IGF1, IL-6, IL-2NLR, PLR and the severity of MPP was analyzed. IL-2, NLR, and PLR significantly increased. The IGF1 in MPP group was lower than control group (P <0.05). IL-6 level in two group was no significant change. NLR, PLR and IL-2 were negatively correlated with IGF1. NLR, IL-2, PLR were positively correlated with MPP severity (P <0.05). NLR, PLR, and IL-2 were upregulated, whereas IGF1 was declined in MPP, which can be used to evaluate the progression of MPP.
支原体肺炎(Mycoplasma pneumonia, MPP)属于非典型肺炎,由肺炎支原体感染引起,占儿童社区肺炎的10-40%。这在学龄前儿童中更为常见。MPP的临床症状多种多样,且难以治愈。本研究分析炎症因子在MPP、中性粒细胞/淋巴细胞比值(NLR)、胰岛素样生长因子1 (IGF1)中的表达。目的是为该病的治疗和诊断提供相关依据。选取正常儿童40例作为对照组。选取78例MPP患儿作为观察组。检测外周血白细胞介素-6 (IL-6)、白细胞介素-2 (IL-2)水平。检测血小板/淋巴细胞比值(PLR)和NLR。ELISA法检测IGF1的表达。分析IGF1、IL-6、IL-2NLR、PLR与MPP严重程度的相关性。IL-2、NLR、PLR显著升高。MPP组IGF1低于对照组(P <0.05)。两组患者IL-6水平无明显变化。NLR、PLR、IL-2与IGF1呈负相关。NLR、IL-2、PLR与MPP严重程度呈正相关(P <0.05)。NLR、PLR和IL-2在MPP中上调,而IGF1在MPP中下降,可用于评估MPP的进展。
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引用次数: 0
Novel nano-SiRNA delivery system loaded with anti-ESR1 siRNA and its application as a cyclosporine drug carrier in dry eye caused by diabetes 装载抗ESR1 siRNA的新型纳米SiRNA递送系统及其作为环孢素药物载体在糖尿病所致干眼症中的应用
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2561
Jing He, Yunzhi Lin, Fen Ye, Ying Gao, Ting Yu, Bilian Ke, Weihong Zhou
Dry eye is a relatively common clinical condition caused by abnormal fluid dynamics and tear quality, for which effective pharmacological treatment is lacking. In this study, a new nano-siRNA delivery system loaded with anti-ESR1 siRNA was designed and synthesized, and its effect in the treatment of dry eye was evaluated. The system significantly inhibited the NaCl-induced increase in inflammatory factors, thereby suppressing the inflammatory response. In addition, the system downregulated the expression level of MMP-9 and STRA6. This system could be developed as a drug for the treatment of diabetes-induced dry eye.
干眼症是一种较为常见的临床疾病,由异常的流体动力学和泪液质量引起,缺乏有效的药物治疗。本研究设计并合成了一种新型的纳米siRNA递送系统,负载抗esr1 siRNA,并对其治疗干眼症的效果进行了评价。该系统显著抑制了nacl诱导的炎症因子的增加,从而抑制了炎症反应。此外,该系统下调了MMP-9和STRA6的表达水平。该系统可开发为治疗糖尿病性干眼症的药物。
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引用次数: 0
Effect of metformin nanoemulsion through AMP-activated protein kinase (AMPK)-mediated autophagy on diabetic neuropathy 二甲双胍纳米乳剂通过 AMP 激活蛋白激酶 (AMPK) 介导的自噬作用对糖尿病神经病变的影响
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2560
Fengmin Liu, Siyun Wang, Xiaojuan Du, Diya Xie
Metformin (MET) is the preferred first-line treatment for patients with type 2 diabetes. However, the mechanism of diabetic peripheral neuropathy (DPN) is still unclear. To improve the oral utilization of metformin, a metformin nanoemulsion (MET-NE) was prepared to investigate its effects on DPN and its underlying mechanism. In this study, a DPN model was established in Wistar rats induced by streptozotocin (STZ). The diabetic rats were randomly divided into four groups: the diabetic model group (DM group), the metformin tablet-treated group (MET group), the metformin nanoemulsion-treated group (MET-NE group), and a normal control group consisting of five normal Wistar rats. All groups were administered the treatment orally for a period of 10 weeks. The findings of the study demonstrated that both MET and MET-NE significantly reduced blood glucose levels, glycated serum protein levels, food intake, and water intake in DM rats. It was also observed that MET-NE was more effective than MET in reducing blood glucose levels. Additionally, both MET and MET-NE treatments significantly increased the motor nerve conduction velocity (MNCV), sensory nerve conduction velocity (SNCV), and sensory nerve action potential (SNAP) amplitude in DM rats. Furthermore, these treatments improved mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL), resulting in a reduced sensitivity to pain stimuli. Moreover, both MET and MET-NE treatments promoted the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) proteins, as well as increased the activity of autophagic proteins in the sciatic nerve. However, no significant differences were observed between MET and MET-NE treatments in terms of these effects. In conclusion, the MET-NE demonstrated a rapid decrease in blood glucose levels and improved glucose tolerance and metabolism, which was found to be superior to MET. Furthermore, MET-NE significantly improved the neurophysiological function and sciatic nerve pain threshold in DPN rats. These beneficial effects may be attributed to the regulation of AMPK-mediated autophagy by MET-NE.
二甲双胍(MET)是2型糖尿病患者首选的一线治疗药物。然而,糖尿病周围神经病变(DPN)的发病机制尚不清楚。为了提高二甲双胍的口服利用率,制备了二甲双胍纳米乳(MET-NE),研究其对DPN的影响及其作用机制。本研究采用链脲佐菌素(STZ)诱导Wistar大鼠建立DPN模型。将糖尿病大鼠随机分为糖尿病模型组(DM组)、二甲双胍片治疗组(MET组)、二甲双胍纳米乳治疗组(MET- ne组)和正常Wistar大鼠5只的正常对照组。各组均给予口服治疗,疗程为10周。研究结果表明,MET和MET- ne均能显著降低糖尿病大鼠的血糖水平、糖化血清蛋白水平、食物摄入量和水摄入量。还观察到MET- ne在降低血糖水平方面比MET更有效。此外,MET和MET- ne处理均显著提高DM大鼠运动神经传导速度(MNCV)、感觉神经传导速度(SNCV)和感觉神经动作电位(SNAP)振幅。此外,这些治疗改善了机械戒断阈值(MWT)和热戒断潜伏期(TWL),从而降低了对疼痛刺激的敏感性。此外,MET和MET- ne处理均促进了amp活化蛋白激酶(AMPK)和乙酰辅酶a羧化酶(ACC)蛋白的磷酸化,并增加了坐骨神经自噬蛋白的活性。然而,MET和MET- ne处理在这些效果方面没有显著差异。综上所述,MET- ne能迅速降低血糖水平,改善葡萄糖耐量和代谢,优于MET。此外,MET-NE显著改善DPN大鼠的神经生理功能和坐骨神经痛阈。这些有益作用可能归因于MET-NE对ampk介导的自噬的调节。
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引用次数: 0
Construction of a bearing capacity testing model for reinforced bridges based on material performance deterioration 构建基于材料性能劣化的加固桥梁承载能力测试模型
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2556
Xia Zhang, Lei Zhang, Rongbin Huang, Xianghui Zhang
Reinforced concrete beam bridges have been extensively utilized in transportation engineering due to their advantages such as simplified material selection and low cost. However, the mechanical performance of steel bars and concrete deteriorates over time due to factors such as prolonged bridge service life, fluctuations in environmental temperature and humidity, and other influences. To achieve a precise and effective prediction of the bearing capacity of reinforced concrete structures, this study proposes a method for assessing bearing capacity in the context of material performance degradation. The study commenced by examining the factors that impact the degradation of bridge performance and subsequently utilized material performance test values along with predicted and corrected values to estimate the reduced bearing capacity of the bridge. Additionally, the mechanical and bonding properties of modified reinforced concrete materials were calculated. The experiment results demonstrate that the calculated values from the modified model closely align with the measured values with a differential range of 0.06 to 0.38. At a micro level, nano-SiO2 modification enhances rubber concrete by improving the compactness of the matrix and enhancing bond strength between steel fiber-and-nanosilica-reinforced crumb rubber concrete and deformed steel bars. The revised model in this study exhibits excellent predictive capability for concrete strength, thereby enhancing the accuracy of outcomes in evaluating bridge technical conditions. This method holds potential for practical engineering applications and scientific research on bridge evaluation.
钢筋混凝土梁桥以其选材简便、造价低廉等优点在交通运输工程中得到了广泛的应用。然而,由于桥梁使用寿命延长、环境温度和湿度波动等因素的影响,钢筋和混凝土的力学性能会随着时间的推移而恶化。为了准确有效地预测钢筋混凝土结构的承载力,本研究提出了一种材料性能退化情况下的承载力评估方法。该研究首先检查了影响桥梁性能退化的因素,随后利用材料性能测试值以及预测和修正值来估计桥梁的承载能力降低。此外,还计算了改性钢筋混凝土材料的力学性能和粘结性能。实验结果表明,修正模型的计算值与实测值基本一致,差值范围为0.06 ~ 0.38。在微观层面上,纳米二氧化硅改性通过改善基体的密实度和增强钢纤维-纳米二氧化硅增强橡胶混凝土颗粒与变形钢筋之间的粘结强度来增强橡胶混凝土。修正后的模型对混凝土强度具有较好的预测能力,从而提高了桥梁技术状况评估结果的准确性。该方法具有实际工程应用和桥梁评价科学研究的潜力。
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引用次数: 0
Management of nerve injury by curcumin after sevoflurane anesthesia in gastric cancer through MAPK signaling pathway 姜黄素通过 MAPK 信号通路控制七氟醚麻醉后胃癌患者的神经损伤
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2545
Jianguang Ren, Ben Cai
Currently, surgery is the only treatment that can completely remove gastric tumor. This study investigated the effect of curcumin on sevoflurane anesthesia-induced nerve damage in rats with gastric cancer (GC). A rat GC model was established and received sevoflurane for anesthesia. The rats were then divided into model group, low-dose (20 mg/kg), high-dose (60 mg/kg) group and blank control group (n = 5, each group). To identify the interaction between curcumin and mitogen-activated protein kinase (MAPK) expression, we set up MAPK mimic group, MAPK inhibitor group, and high-dose curcumin+MAPK inhibitor group (n = 5). The cognitive ability of rats after anesthesia and neuronal damage was assessed using Morris water maze test, whilst the expressions of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and pyroptosis were also detected. Administration of curcumin attenuated neuronal injury and pyroptosis in the hippocampus induced by sevoflurane, and facilitated the recovery of memory impairment in rats, resulting in decreased expression of MAPK and increased expressions of BNDF and NGF. After treatment with MAPK inhibitors, the nerve damage in the rat hippocampus tissue was controlled, and more prominently neuroprotective effect appeared in the curcumin high-dose+MAPK inhibitor group. Curcumin can thus effectively up-regulate BNDF and NGF in hippocampal tissue, which is closely related to inhibited MAPK pathway activity. Curcumin protects the nervous system by inhibiting the expression of pyroptin, contributing toimprovement of cognitive impairment in rats.
目前,手术是唯一可以完全切除胃肿瘤的治疗方法。本研究探讨了姜黄素对七氟醚麻醉致胃癌大鼠神经损伤的影响。建立大鼠GC模型,给予七氟醚麻醉。将大鼠分为模型组、低剂量组(20 mg/kg)、高剂量组(60 mg/kg)和空白对照组(每组5只)。为了确定姜黄素与丝裂原活化蛋白激酶(MAPK)表达的相互作用,我们设置MAPK模拟组、MAPK抑制剂组和高剂量姜黄素+MAPK抑制剂组(n = 5),采用Morris水迷宫法检测麻醉后大鼠的认知能力和神经元损伤,同时检测脑源性神经营养因子(BDNF)、神经生长因子(NGF)和焦凋亡的表达。姜黄素可减轻七氟醚诱导的海马神经元损伤和焦亡,促进记忆障碍大鼠的恢复,导致MAPK表达降低,BNDF和NGF表达增加。经MAPK抑制剂治疗后,大鼠海马组织神经损伤得到控制,姜黄素高剂量+MAPK抑制剂组神经保护作用更为显著。因此,姜黄素可以有效上调海马组织中的BNDF和NGF,这与抑制MAPK通路活性密切相关。姜黄素通过抑制焦肽的表达来保护神经系统,有助于改善大鼠的认知障碍。
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引用次数: 0
Preparation of functionalized polymer nanomaterials and application in renal injury 功能化聚合物纳米材料的制备及其在肾损伤中的应用
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2554
Qin Liu
Renal injury, which is a prevalent condition, significantly impacts the health of competitive wrestlers. However, there is a limited number of therapeutic methods and drugs available for its treatment. To tackle this issue, a renal targeted drug based on functionalized polymer nanoparticles (FPNPs) is being studied. The primary methods in the preparation of FPNPs involve utilizing the thin film hydration technique to create nanoparticles and encapsulating the drug TP within them as a treatment for renal injury, thus forming TP-FPNPs. Subsequently, the renal targeting of TP-FPNPs is analyzed using in vitro organ fluorescence imaging techniques. Furthermore, a renal IRI model is constructed to assess the pharmacokinetics of TP-FPNPs using the application method. The preparation results of TP-FPNPs reveal a hydrated particle size of approximately 90 nm, which remains in the renal region for over 48 hours. Additionally, the concentration content surpasses that of other organs by more than threefold after 12 hours. Moreover, in the application results, TP-FPNPs continue to possess a concentration of 302.5 ng/g even after 48 hours post-injection. Based on the aforementioned results, it can be concluded that TP-FPNPs exhibit specific targeting, biocompatibility, and an extended retention time. Thus, this study is expected to effectively achieve the effect of treating renal injury in martial arts athletes, establishing an experimental foundation for its clinical treatment.
肾脏损伤,这是一个普遍的条件,显著影响健康的竞技摔跤手。然而,用于治疗的治疗方法和药物数量有限。为了解决这一问题,一种基于功能化聚合物纳米颗粒(FPNPs)的肾脏靶向药物正在研究中。制备FPNPs的主要方法是利用薄膜水合技术制造纳米颗粒,并将药物TP包封在其中,从而形成TP-FPNPs,作为肾损伤的治疗方法。随后,利用体外器官荧光成像技术分析TP-FPNPs的肾脏靶向性。此外,构建肾脏IRI模型,采用应用方法评估TP-FPNPs的药代动力学。TP-FPNPs的制备结果显示,水合颗粒尺寸约为90 nm,在肾区停留超过48小时。另外,12小时后浓度含量超过其他器官3倍以上。此外,在应用结果中,TP-FPNPs在注射后48小时仍保持302.5 ng/g的浓度。基于上述结果,TP-FPNPs具有特异性靶向性、生物相容性和较长的滞留时间。因此,本研究有望有效达到治疗武术运动员肾损伤的效果,为其临床治疗奠定实验基础。
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引用次数: 0
Total glucosides of peony regulate toll-like receptor to inhibit inflammatory response in diabetic nephropathy 牡丹总苷调节收费样受体,抑制糖尿病肾病的炎症反应
IF 0.7 4区 材料科学 Q3 Materials Science Pub Date : 2023-12-01 DOI: 10.1166/mex.2023.2568
Lang Li, Huan Wang, Chunyu Zhao
Diabetic nephropathy (DN) is a common chronic disease affecting people’s life. Total glucosides of peony (TGP) regulates TLR4/NF-κB activation. This study aims at investigating the underlying mechanism of TGP in DN treatment. A retrospective analysis of clinical data was conducted to observe periodic acid-silver metheramine (PASM) staining and detect the expression of TLR4 and VEGF in DN. Additionally, rats were injected with Streptozocin (STZ) (30–60 mg) according to the ratio of 45–65 mg/kg to establish DN model. 8 weeks later, rats of experimental group were intraperitoneally injected with TGP. Kidney was collected for HE staining to observe morphological changes. Fibronectin expression was detected by histochemistry and the level of TLR4/NF-κB pathway-related proteins and apoptosis were detected by Western blot. PASM staining revealed focal tubular atrophy and interstitial fibrosis in DN patients. The renal medulla gradually disappeared and infiltration increased in control group, while inflammatory cells decreased in experimental group. The expression of fibronectin, TLR4 and p-p65 was decreased after TGP treatment. TGP treatment significantly decreased fibronectin expression and TGP treatment-induced inhibition of NF-κB signaling enhanced apoptotic activation of HK-2 cells, which was partially reversed by TLR4 and NF-κB inhibitors. TGP can inhibit inflammatory response of DN via regulating TLR4/NF-κB.
糖尿病肾病(DN)是影响人们生活的常见慢性疾病。牡丹总糖苷(TGP)调控TLR4/NF-κB的活化。本研究旨在探讨TGP在DN治疗中的潜在机制。回顾性分析临床资料,观察周期性酸-甲基胺银(PASM)染色,检测TLR4、VEGF在DN中的表达。并按45 ~ 65 mg/kg的比例注射链脲佐菌素(STZ) 30 ~ 60 mg建立DN模型。8周后,实验组大鼠腹腔注射TGP。取肾脏进行HE染色,观察肾脏形态学变化。组织化学法检测纤维连接蛋白表达,Western blot法检测TLR4/NF-κB通路相关蛋白及凋亡水平。PASM染色显示DN患者局灶性小管萎缩和间质纤维化。对照组肾髓质逐渐消失,浸润增多,实验组炎症细胞减少。TGP处理后,纤维连接蛋白、TLR4和p-p65的表达均降低。TGP处理显著降低了纤维连接蛋白的表达,TGP处理诱导的NF-κB信号的抑制增强了HK-2细胞的凋亡激活,这被TLR4和NF-κB抑制剂部分逆转。TGP可通过调节TLR4/NF-κB抑制DN的炎症反应。
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引用次数: 0
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Materials Express
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