虾青素对D-半乳糖致衰老大鼠肾脏和心脏组织氧化损伤的修复作用

通过建立D-半乳糖致衰老模型,研究虾青素对衰老大鼠肾脏和心脏组织氧化损伤的修复作用。实验设空白组、模型组、虾青素低、中、高（5、10、15 mg/kg）剂量组和二甲双胍（MET）阳性对照组。检测肾脏和心脏系数,肾脏和心脏组织中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力和丙二醛（MDA）含量等指标,观测苏木精-伊红染色（HE）病理组织切片。结果表明,与模型组相比,虾青素能改善D-半乳糖造成的肾脏和心脏系数下降,减少肾脏和心脏组织中MDA含量,并显著提高抗氧化物酶（SOD、CAT、GSH-Px）活力。其中,高剂量组（15 mg/kg）大鼠肾脏和心脏中MDA含量显著降低了70.48%和38.02%（p<0.01）,对于SOD、CAT和GSH-Px活力,肾脏中分别提高了37.22%、43.73%和52.01%（p<0.01）,心脏中分别提高了85.47%、52.08%和64.77%（p<0.01）。病理切片显示虾青素能有效缓解肾脏和心脏组织的氧化损伤。以上结果全面揭示虾青素能通过减轻氧化应激来抑制衰老大鼠肾脏和心脏组织的损伤,其机制可能与抗氧化有关。     

Evaluating the Effects of Subnormothermic Perfusion with AP39 in a Novel Blood-Free Model of Ex Vivo Kidney Preservation and Reperfusion

The use of blood for normothermic and subnormothermic kidney preservation hinders the translation of these approaches and promising therapeutics. This study evaluates whether adding hydrogen sulfide donor AP39 to Hemopure, a blood substitute, during subnormothermic perfusion improves kidney outcomes. After 30 min of renal pedicle clamping, porcine kidneys were treated to 4 h of static cold storage (SCS-4 °C) or subnormothermic perfusion at 21 °C with Hemopure (H-21 °C), Hemopure + 200 nM AP39 (H200nM-21 °C) or Hemopure + 1 µM AP39 (H1µM-21 °C). Then, kidneys were reperfused with Hemopure at 37 °C for 4 h with metabolic support. Perfusate composition, tissue oxygenation, urinalysis and histopathology were analyzed. During preservation, the H200nM-21 °C group exhibited significantly higher urine output than the other groups and significantly higher tissue oxygenation than the H1µM-21 °C group at 1 h and 2h. During reperfusion, the H200nM-21 °C group exhibited significantly higher urine output and lower urine protein than the other groups. Additionally, the H200nM-21 °C group exhibited higher perfusate pO₂ levels than the other groups and significantly lower apoptotic injury than the H-21 °C and the H1µM-21 °C groups. Thus, subnormothermic perfusion at 21 °C with Hemopure + 200 nM AP39 improves renal outcomes. Additionally, our novel blood-free model of ex vivo kidney preservation and reperfusion could be useful for studying other therapeutics.     

龙眼叶水提物抗实验性肾结石作用的研究

为了研究龙眼叶水提取物对肾结石模型大鼠的抑制作用,采用灌胃乙二醇+氯化铵溶液建立肾结石大鼠模型,造模成功后,用低、中、高不同剂量的龙眼叶水提取物对小鼠进行治疗恢复,测定24 h饮水量和尿量、尿常规指标、以及血清Cr、BUN、UA、Ca~(2+)、Mg~(2+)、草酸水平,肾组织中Ca~(2+)、Mg~(2+)、草酸水平,观察肾脏病理学改变及结晶情况。结果表明:与模型组相比较,各剂量龙眼叶水提取物能降低大鼠24 h饮水量(p0.05)各剂量提取物均能降低模型大鼠24 h尿液草酸水平,其中高剂量组上述二者达到显著性差异(p0.05);各剂量提取物均能显著降低血清中尿酸(UA)、尿素氮(BUN)、肌酐(Cr)浓度,而对血清中的Ca~(2+)、Mg~(2+)浓度影响不明显,但能显著降低肾脏中Mg~(2+)浓度。各剂量龙眼叶水提取物能不同程度降低肾脏器系数和肾脏草酸水平,减轻肾小管上皮细胞凋亡及草酸结晶程度,改善肾脏病变,降低肾结石发生率。研究结果显示龙眼叶水提取物能抑制肾结石的发生。     

蜂胶提取物对顺铂诱导大鼠肝、肾损伤的保护作用

目的：探究蜂胶乙醇提取物对顺铂所致肝、肾损伤的干预作用。方法：采用不同剂量（50、100、 150 mg/kg mb）的蜂胶乙醇提取物对大鼠进行灌胃,连续7 d给药后单次腹腔注射10 mg/kg mb的顺铂建立肝、肾损伤 模型,之后再灌胃5 d。实验结束后通过测定血清中肝、肾损伤的标志物,肝、肾组织中脂质过氧化物、抗氧化物 的含量以及观察肝、肾组织病理学的改变来探究蜂胶对顺铂毒性的干预作用。结果：与模型组相比,高剂量组大鼠 血清中谷草转氨酶、谷丙转氨酶的活力,尿素氮、肌酐含量均有降低;肝、肾组织中超氧化物歧化酶、过氧化氢酶 的活力,还原型谷胱甘肽的含量均有升高;丙二醛、诱导型一氧化氮合酶含量均有降低;从组织病理学方面来看, 模型组的肝、肾组织都出现了病变,表现为肝小叶细胞坏死,肾小球细胞脱落、空泡性等,蜂胶给药组这些病变情 况均有不同程度的降低。结论：蜂胶乙醇提取物可以降低体内的氧化应激程度,提高机体自身抗氧化能力,从而很 好地降低顺铂造成的肝、肾损伤。     

高能辐照下环氧树脂对腰形碳纤维的表面改性

利用高能射线共辐照接枝,在环氧树脂/丙酮溶液中对腰形截面碳纤维表面进行了处理.通过扫描电子显微镜(SEM)观察了纤维的表面及复合材料断口形貌的变化;利用浸润性测试方法分析了纤维表面能的变化;采用X射线光电子能谱(XPS)方法分析了纤维表面化学元素及官能团的组成;通过层间剪切强度(ILSS)表征了纤维增强环氧树脂复合材料的界面性能.结果表明,处理后碳纤维表面沟槽变深,氧元素和碳元素百分含量比(O/C)提高,表面能极性分量增加,ILSS最大可提高18.3%,达到91.3MPa.     

Ferroptosis: A Potential Therapeutic Target in Acute Kidney Injury

Ferroptosis is a recently recognized form of nonapoptotic cell death that is triggered by reactive oxidative species (ROS) due to iron overload, lipid peroxidation accumulation, or the inhibition of phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Recent studies have reported that ferroptosis plays a vital role in the pathophysiological process of multiple systems such as the nervous, renal, and pulmonary systems. In particular, the kidney has higher rates of O₂ consumption in its mitochondria than other organs; therefore, it is susceptible to imbalances between ROS and antioxidants. In ischemia/reperfusion (I/R) injury, which is damage caused by the restoring blood flow to ischemic tissues, the release of ROS and reactive nitrogen species is accelerated and contributes to subsequent inflammation and cell death, such as ferroptosis, as well as apoptosis and necrosis being induced. At the same time, I/R injury is one of the major causes of acute kidney injury (AKI), causing significant morbidity and mortality. This review highlights the current knowledge on the involvement of ferroptosis in AKI via oxidative stress.     

Potential Renal Damage Biomarkers in Alport Syndrome—A Review of the Literature

Alport syndrome (AS) is the second most common cause of inherited chronic kidney disease. This disorder is caused by genetic variants on COL4A3, COL4A4 and COL4A5 genes. These genes encode the proteins that constitute collagen type IV of the glomerular basement membrane (GBM). The heterodimer COL4A3A4A5 constitutes the majority of the GBM, and it is essential for the normal function of the glomerular filtration barrier (GFB). Alterations in any of collagen type IV constituents cause disruption of the GMB structure, allowing leakage of red blood cells and albumin into the urine, and compromise the architecture of the GFB, inducing inflammation and fibrosis, thus resulting in kidney damage and loss of renal function. The advances in DNA sequencing technologies, such as next-generation sequencing, allow an accurate diagnose of AS. Due to the important risk of the development of progressive kidney disease in AS patients, which can be delayed or possibly prevented by timely initiation of therapy, an early diagnosis of this condition is mandatory. Conventional biomarkers such as albuminuria and serum creatinine increase relatively late in AS. A panel of biomarkers that might detect early renal damage, monitor therapy, and reflect the prognosis would have special interest in clinical practice. The aim of this systematic review is to summarize the biomarkers of renal damage in AS as described in the literature. We found that urinary Podocin and Vascular Endothelial Growth Factor A are important markers of podocyte injury. Urinary Epidermal Growth Factor has been related to tubular damage, interstitial fibrosis and rapid progression of the disease. Inflammatory markers such as Transforming Growth Factor Beta 1, High Motility Group Box 1 and Urinary Monocyte Chemoattractant Protein- 1 are also increased in AS and indicate a higher risk of kidney disease progression. Studies suggest that miRNA-21 is elevated when renal damage occurs. Novel techniques, such as proteomics and microRNAs, are promising.