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Does Microwave Exposure at Different Doses in the Pre/Postnatal Period Affect Growing Rat Bone Development? 产前/产后不同剂量的微波暴露会影响生长期大鼠的骨骼发育吗?
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-11 DOI: 10.33549/physiolres.935148
A Karadayi, H Sarsmaz, A Çigel, B Engiz, N Ünal, S Ürkmez, S Gürgen

Effects of pre/postnatal 2.45 GHz continuous wave (CW), Wireless-Fidelity (Wi-Fi) Microwave (MW) irradiation on bone have yet to be well defined. The present study used biochemical and histological methods to investigate effects on bone formation and resorption in the serum and the tibia bone tissues of growing rats exposed to MW irradiation during the pre/postnatal period. Six groups were created: one control group and five experimental groups subjected to low-level different electromagnetic fields (EMF) of growing male rats born from pregnant rats. During the experiment, the bodies of all five groups were exposed to 2.45 GHz CW-MW for one hour/day. EMF exposure started after fertilization in the experimental group. When the growing male rats were 45 days old in the postnatal period, the control and five experimental groups' growing male and maternal rats were sacrificed, and their tibia tissues were removed. Maternal rats were not included in the study. No differences were observed between the control and five experimental groups in Receptor Activator Nuclear factor-kB (RANK) biochemical results. In contrast, there was a statistically significant increase in soluble Receptor Activator of Nuclear factor-kB Ligand (sRANKL) and Osteoprotegerin (OPG) for 10 V/m and 15 V/m EMF values. Histologically, changes in the same groups supported biochemical results. These results indicate that pre/postnatal exposure to 2.45 GHz EMF at 10 and 15 V/m potentially affects bone development.

产前/产后2.45 GHz连续波(CW)、无线保真(Wi-Fi)微波(MW)辐照对骨骼的影响尚未明确。本研究采用生化和组织学方法,研究了微波辐照对出生前/后生长期大鼠血清和胫骨骨组织中骨形成和骨吸收的影响。实验共分六组:一组为对照组,五组为实验组,实验对象均为孕鼠所生的生长期雄性大鼠,均受到低水平不同电磁场(EMF)的影响。在实验过程中,所有五组的身体每天暴露在 2.45 千兆赫的 CW-MW 中一小时。实验组在受精后开始接触电磁场。对照组和五个实验组的生长期雄鼠和母鼠在产后 45 天时被处死,并取出胫骨组织。母鼠不参与研究。对照组和五个实验组的受体活化因子核因子-kB(RANK)生化结果无差异。相反,在 10 伏/米和 15 伏/米电磁场值下,可溶性核因子-kB 受体活化因子配体(sRANKL)和骨蛋白激酶(OPG)在统计学上有显著增加。从组织学角度看,同组的变化支持生化结果。这些结果表明,产前/产后暴露于 10 伏/米和 15 伏/米的 2.45 千兆赫电磁场可能会影响骨骼发育。
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引用次数: 0
Resveratrol Attenuates Rheumatoid Arthritis Induce Neutrophil Extracellular Traps via TLR-4 Mediated Inflammation in C57BL/6 Mice. 白藜芦醇通过TLR-4介导的炎症减轻C57BL/6小鼠类风湿性关节炎诱导的中性粒细胞胞外捕获器的作用
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935172
Zequan Chen, Guowei Xiao, AO Jian
The objective of this study was to evaluate whether RSV inhibits neutrophil extracellular traps (NETs) that induce joint hyperalgesia in C57BL/6 mice after adjuvant-induced arthritis. A subplantar injection of Freund's complete adjuvant was administered to C57BL/6 mice on day 0 for immunization in the AIA model. Resveratrol (RSV, 25 mg/kg) was administered intraperitoneally once daily starting on day 22 and continuing for two weeks. The effects of mechanical hyperalgesia and edema formation have been assessed in addition to histopathological scoring. Mice were sacrificed on day 35 to determine cytokine levels and PADI4 and COX-2 expression levels. ELISA was used to quantify neutrophil extracellular traps (NETs) along with neutrophil elastase-DNA and myeloperoxidase-DNA complexes in neutrophils. An immunohistochemical stain was performed on knee joints to determine the presence of nuclear factor kappa B p65 (NF-kappaB p65). AIA mice were found to have higher levels of NET in joints and their joint cells demonstrated an increased expression of the PADI4 gene. Treatment with RSV in AIA mice (25 mg/kg, i.p.) significantly (P<0.05) inhibited joint hyperalgesia, resulting in a significant increase in mechanical threshold, a decrease in articular edema, a decrease in the production of inflammatory cytokines, increased COX-2 expression, and a decrease in the immunostaining of NF-kappaB. Furthermore, treatment with RSV significantly reduced the amount of neutrophil elastase (NE)-DNA and MPO-DNA complexes, which were used as indicators of NET formation (P<0.05). This study indicates that RSV reduces NET production and hyperalgesia by reducing inflammation mediated by PADI4 and COX-2. According to these data, NETs contribute to joint pain and resveratrol can be used to treat pain in RA through this pathway.
本研究的目的是评估 RSV 是否会抑制中性粒细胞胞外捕获物(NET),而中性粒细胞胞外捕获物会诱发 C57BL/6 小鼠在佐剂诱导的关节炎后出现关节痛觉减退。在AIA模型免疫的第0天,给C57BL/6小鼠注射弗罗因德完全佐剂(Freund's complete adjuvant)。从第22天开始腹腔注射白藜芦醇(RSV,25 mg/kg),每天一次,持续两周。除组织病理学评分外,还评估了机械性痛觉减退和水肿形成的影响。小鼠在第 35 天被处死,以确定细胞因子水平以及 PADI4 和 COX-2 的表达水平。用酶联免疫吸附法(ELISA)量化中性粒细胞胞外捕获物(NET)以及中性粒细胞中的中性粒细胞弹性蛋白酶-DNA 和髓过氧化物酶-DNA 复合物。对膝关节进行免疫组化染色,以确定核因子卡巴B p65(NF-kappaB p65)的存在。结果发现,AIA 小鼠关节中的 NET 含量较高,其关节细胞中 PADI4 基因的表达量也有所增加。用 RSV 治疗 AIA 小鼠(25 mg/kg,i.p.)可显著(P<0.05)抑制关节超痛感,从而显著提高机械阈值,减少关节水肿,减少炎性细胞因子的产生,增加 COX-2 的表达,减少 NF-kappaB 的免疫染色。此外,用 RSV 治疗还能显著减少中性粒细胞弹性蛋白酶(NE)-DNA 和 MPO-DNA 复合物的数量,这些复合物是 NET 形成的指标(P<0.05)。这项研究表明,RSV 可通过减少 PADI4 和 COX-2 介导的炎症来减少 NET 的产生和痛觉减退。根据这些数据,NET 可导致关节疼痛,白藜芦醇可通过这一途径治疗 RA 疼痛。
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引用次数: 0
Angiotensin I and II Stimulate Cell Invasion of SARS-CoV-2: Potential Mechanism via Inhibition of ACE2 Arm of RAS. 血管紧张素 I 和 II 刺激 SARS-CoV-2 的细胞侵袭:通过抑制 RAS 的 ACE2 臂的潜在机制
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935198
S. Zorad, M. Skrabanova, M. Zilkova, M. Cente, N. Turic Csokova, B. Kovacech, D. Cizkova, P. Filipcik
Angiotensin-converting enzyme 2 (ACE2), one of the key enzymes of the renin-angiotensin system (RAS), plays an important role in SARS-CoV-2 infection by functioning as a virus receptor. Angiotensin peptides Ang I and Ang II, the substrates of ACE2, can modulate the binding of SARS-CoV-2 Spike protein to the ACE2 receptor. In the present work, we found that co incubation of HEK-ACE2 and Vero E6 cells with the SARS-CoV-2 Spike pseudovirus (PVP) resulted in stimulation of the virus entry at low and high micromolar concentrations of Ang I and Ang II, respectively. The potency of Ang I and Ang II stimulation of virus entry corresponds to their binding affinity to ACE2 catalytic pocket with 10 times higher efficiency of Ang II. The Ang II induced mild increase of PVP infectivity at 20 microM; while at 100 microM the increase (129.74+/-3.99 %) was highly significant (p<0.001). Since the angiotensin peptides act in HEK ACE2 cells without the involvement of angiotensin type I receptors, we hypothesize that there is a steric interaction between the catalytic pocket of the ACE2 enzyme and the SARS-CoV-2 S1 binding domain. Oversaturation of the ACE2 with their angiotensin substrate might result in increased binding and entry of the SARS-CoV-2. In addition, the analysis of angiotensin peptides metabolism showed decreased ACE2 and increased ACE activity upon SARS-CoV-2 action. These effects should be taken into consideration in COVID-19 patients suffering from comorbidities such as the over-activated renin-angiotensin system as a mechanism potentially influencing the SARS-CoV-2 invasion into recipient cells.
血管紧张素转换酶 2(ACE2)是肾素-血管紧张素系统(RAS)的关键酶之一,它作为病毒受体在 SARS-CoV-2 感染中发挥着重要作用。血管紧张素肽 Ang I 和 Ang II 是 ACE2 的底物,可调节 SARS-CoV-2 Spike 蛋白与 ACE2 受体的结合。在本研究中,我们发现将 HEK-ACE2 细胞和 Vero E6 细胞与 SARS-CoV-2 Spike 伪病毒(PVP)共培养,在低、高微摩尔浓度的 Ang I 和 Ang II 的作用下,可分别刺激病毒的进入。Ang I和Ang II刺激病毒进入的效力与它们与ACE2催化口袋的结合亲和力有关,Ang II的效率是ACE2的10倍。在 20 微摩尔时,血管紧张素Ⅱ诱导的 PVP 感染性轻微增加;而在 100 微摩尔时,这种增加(129.74+/-3.99 %)非常显著(p<0.001)。由于血管紧张素肽在 HEK ACE2 细胞中发挥作用时没有血管紧张素 I 型受体的参与,我们推测 ACE2 酶的催化口袋与 SARS-CoV-2 S1 结合域之间存在立体相互作用。ACE2 与其血管紧张素底物的过饱和可能会导致 SARS-CoV-2 的结合和进入增加。此外,血管紧张素肽代谢分析表明,在 SARS-CoV-2 作用下,ACE2 活性降低,ACE 活性增加。对于患有合并症(如肾素-血管紧张素系统过度激活)的 COVID-19 患者,应将这些影响作为可能影响 SARS-CoV-2 侵入受体细胞的机制加以考虑。
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引用次数: 0
Skeletal Muscle Electrical Stimulation Prevents Progression of Disuse Muscle Atrophy via Forkhead Box O Dynamics Mediated by Phosphorylated Protein Kinase B and Peroxisome Proliferator-Activated Receptor gamma Coactivator-1alpha. 骨骼肌电刺激通过磷酸化蛋白激酶 B 和过氧化物酶体增殖体激活受体 gamma 辅激活剂-1alpha 介导的叉头框 O 动态变化,防止废用性肌肉萎缩的进展。
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935157
Ayumi Takahashi, Y. Honda, N. Tanaka, Jyunpei Miyake, Shunsuke Maeda, H. Kataoka, Junya Sakamoto, Minoru Okita, P. -. 1. •. FoxO
Although electrical muscle stimulation (EMS) of skeletal muscle effectively prevents muscle atrophy, its effect on the breakdown of muscle component proteins is unknown. In this study, we investigated the biological mechanisms by which EMS-induced muscle contraction inhibits disuse muscle atrophy progression. Experimental animals were divided into a control group and three experimental groups: immobilized (Im; immobilization treatment), low-frequency (LF; immobilization treatment and low-frequency muscle contraction exercise), and high-frequency (HF; immobilization treatment and high-frequency muscle contraction exercise). Following the experimental period, bilateral soleus muscles were collected and analyzed. Atrogin-1 and Muscle RING finger 1 (MuRF-1) mRNA expression levels were significantly higher for the experimental groups than for the control group but were significantly lower for the HF group than for the Im group. Peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) mRNA and protein expression levels in the HF group were significantly higher than those in the Im group, with no significant differences compared to the Con group. Both the Forkhead box O (FoxO)/phosphorylated FoxO and protein kinase B (AKT)/phosphorylated AKT ratios were significantly lower for the Im group than for the control group and significantly higher for the HF group than for the Im group. These results, the suppression of atrogin-1 and MuRF-1 expression for the HF group may be due to decreased nuclear expression of FoxO by AKT phosphorylation and suppression of FoxO transcriptional activity by PGC-1alpha. Furthermore, the number of muscle contractions might be important for effective EMS.
虽然对骨骼肌的肌肉电刺激(EMS)能有效防止肌肉萎缩,但其对肌肉成分蛋白分解的影响尚不清楚。在这项研究中,我们探讨了 EMS 诱导的肌肉收缩抑制废用性肌肉萎缩进展的生物学机制。实验动物分为对照组和三个实验组:固定组(Im;固定治疗)、低频组(LF;固定治疗和低频肌肉收缩运动)和高频组(HF;固定治疗和高频肌肉收缩运动)。实验结束后,收集并分析双侧比目鱼肌。实验组的 Atrogin-1 和肌肉环指 1 (MuRF-1) mRNA 表达水平明显高于对照组,但高频组明显低于 Im 组。HF组的过氧化物酶体增殖激活受体γ辅助激活剂-1α(PGC-1α)mRNA和蛋白表达水平明显高于Im组,与Con组相比无明显差异。Im组的叉头框O(FoxO)/磷酸化FoxO和蛋白激酶B(AKT)/磷酸化AKT比率均明显低于对照组,而HF组则明显高于Im组。这些结果表明,高频组atrogin-1和MuRF-1的表达受到抑制可能是由于AKT磷酸化导致FoxO的核表达减少以及PGC-1α抑制了FoxO的转录活性。此外,肌肉收缩的次数可能对有效的 EMS 非常重要。
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引用次数: 0
Heat Stroke Induces Pyroptosis in Spermatogonia via the cGAS-STING Signaling Pathway. 中暑通过 cGAS-STING 信号途径诱导精原细胞的嗜热症
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935163
Qi-fei Deng, Ying Liu, H. Chu, B. Peng, Xiang Liu, Yong-Sheng Cao, Y.-S. Cao
To explore the mechanism whereby cGAS-STING pathway regulates the pyroptosis of cryptorchidism cells, with a view to finding a new strategy for clinically treating cryptorchidism-induced infertility. Spermatogonial GC-1 cells were heat stimulated to simulate the heat hurt microenvironment of cryptorchidism. The cell viability was assayed by CCK-8, and cellular DNA damage was detected by gamma-H2AX immunofluo-rescence assay. Flow cytometry was employed to assess pyroptosis index, while western blot, ELISA and PCR were used to examine the expressions of pyroptosis-related proteins (Caspase-1, IL-1beta, NLRP3) and cGAS-STING pathway proteins (cGAS, STING). After STING silencing by siRNA, the expressions of pyroptosis-related proteins were determined. Pyroptosis occurred after heat stimulation of cells. Morphological detection found cell swelling and karyopyknosis. According to the gamma-H2AX immunofluorescence (IFA) assay, the endonuclear green fluorescence was significantly enhanced, the gamma-H2AX content markedly increased, and the endonuclear DNA was damaged. Flow cytometry revealed a significant increase in pyroptosis index. Western blot and PCR assays showed that the expressions of intracellular pyrogenic proteins like Caspase-1, NLRP3 and GSDMD were elevated. The increased STING protein and gene expressions in cGAS-STING pathway suggested that the pathway was intracellularly activated. Silencing STING protein in cGAS-STING pathway led to significantly inhibited pyroptosis. These results indicate that cGAS-STING pathway plays an important role in heat stress-induced pyroptosis of spermatogonial cells. After heat stimulation of spermatogonial GC-1 cells, pyroptosis was induced and cGAS-STING pathway was activated. This study can further enrich and improve the molecular mechanism of cryptorchidism.
探索 cGAS-STING 通路调控隐睾症细胞热休克的机制,以期找到临床治疗隐睾症诱发的不育症的新策略。对精原细胞 GC-1 进行热刺激,模拟隐睾症的热损伤微环境。用CCK-8检测细胞活力,用γ-H2AX免疫荧光检测细胞DNA损伤。流式细胞术评估了细胞的嗜热指数,Western印迹、ELISA和PCR检测了嗜热相关蛋白(Caspase-1、IL-1beta、NLRP3)和cGAS-STING通路蛋白(cGAS、STING)的表达。用 siRNA 沉默 STING 后,测定了热休克相关蛋白的表达。热刺激细胞后,细胞发生了嗜热症。形态学检测发现细胞肿胀和核分裂。γ-H2AX免疫荧光(IFA)检测显示,核内绿色荧光明显增强,γ-H2AX含量显著增加,核内DNA受损。流式细胞术显示热核变指数明显增加。Western 印迹和 PCR 检测显示,Caspase-1、NLRP3 和 GSDMD 等细胞内热原蛋白的表达量升高。cGAS-STING 通路中 STING 蛋白和基因表达的增加表明该通路在细胞内被激活。沉默 cGAS-STING 通路中的 STING 蛋白可显著抑制细胞的嗜热反应。这些结果表明,cGAS-STING通路在热应激诱导的精原细胞热凋亡中起着重要作用。对精原细胞GC-1进行热刺激后,诱导了细胞的热凋亡,并激活了cGAS-STING通路。这项研究可进一步丰富和完善隐睾症的分子机制。
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引用次数: 0
Sex-Linked Differences in Cardiac Atrophy After Mechanical Unloading Induced by Heterotopic Heart Transplantation. 异位心脏移植诱发机械性卸载后心脏萎缩的性别差异
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935217
Dushan Michael Kolesar, P. Kujal, I. Mrázová, M. Pokorný, P. Škaroupková, Janusz Sadowski, L. C̆ervenka, Ivan Netuka, M. D. Kolesár
No information is available about sex-related differences in unloading-induced cardiac atrophy. We aimed to compare the course of unloading-induced cardiac atrophy in intact (without gonadectomy) male and female rats, and in animals after gonadectomy, to obtain insight into the influence of sex hormones on this process. Heterotopic heart transplantation (HT((x)) was used as a model for heart unloading. Cardiac atrophy was assessed as the weight ratio of heterotopically transplanted heart weight (HW) to the native HW on days 7 and 14 after HTx in intact male and female rats. In separate experimental groups, gonadectomy was performed in male and female recipient animals 28 days before HT(x) and the course of cardiac atrophy was again evaluated on days 7 and 14 after HT(x). In intact male rats, HT(x) resulted in significantly greater decreases in whole HW when compared to intact female rats. The dynamics of the left ventricle (LV) and right ventricle (RV) atrophy after HT(x) was quite similar to that of whole hearts. Gonadectomy did not have any significant effect on the decreases in whole HW, LV, and RV weights, with similar results in male and female rats. Our results show that the development of unloading-induced cardiac atrophy is substantially reduced in female rats when compared to male rats. Since gonadectomy did not alter the course of cardiac atrophy after HTx, similarly in both male and female rats, we conclude that sex-linked differences in the development of unloading-induced cardiac atrophy are not caused by the activity of sex hormones.
目前还没有关于卸载诱导的心脏萎缩的性别差异的信息。我们的目的是比较完整(未切除性腺)雄性大鼠和雌性大鼠以及切除性腺后的动物在卸载诱导的心脏萎缩过程中的表现,以深入了解性激素对这一过程的影响。异位心脏移植(HT((x))被用作心脏卸载的模型。在完整雄性和雌性大鼠进行异位心脏移植后的第7天和第14天,以异位移植心脏重量(HW)与原生心脏重量之比来评估心脏萎缩情况。在不同的实验组中,雄性和雌性受体动物在 HT(x) 28 天前进行性腺切除,并在 HT(x) 后第 7 天和第 14 天再次评估心脏萎缩的过程。在完整的雄性大鼠中,与完整的雌性大鼠相比,HT(x)导致整个HW的下降幅度明显更大。HT(x)后左心室和右心室萎缩的动态变化与整个心脏的萎缩非常相似。性腺切除对整个HW、左心室和右心室重量的下降没有显著影响,雄性和雌性大鼠的结果相似。我们的研究结果表明,与雄性大鼠相比,雌性大鼠卸载诱导的心脏萎缩的发生率大大降低。由于性腺切除并没有改变 HTx 后心脏萎缩的过程,雄性和雌性大鼠的情况类似,因此我们得出结论,卸载诱导的心脏萎缩发展过程中的性别差异并不是由性激素的活性引起的。
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引用次数: 0
Suppression of microRNA-320 Induces Cerebral Protection Against Ischemia/Reperfusion Injury by Targeting HMGB1/NF-kappaB Axis. 抑制microRNA-320可通过靶向HMGB1/NF-kappaB轴诱导对缺血再灌注损伤的脑保护作用
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-06 DOI: 10.33549/physiolres.935081
S. Liang, W. Cao, Y. Zhuang, D. Zhang, S. Du, H. Shi
MicroRNAs have been shown to potentially function in cerebral ischemia/reperfusion (IR) injury. This study aimed to examine the expression of microRNA-320 (miR-320) in cerebral IR injury and its involvement in cerebral mitochondrial function, oxidative stress, and inflammatory responses by targeting the HMGB1/NF-kappaB axis. Sprague-Dawley rats were subjected to middle cerebral artery occlusion to simulate cerebral IR injury. The cerebral expression of miR-320 was assessed using qRT-PCR. Neurological function, cerebral infarct volume, mitochondrial function, oxidative stress, and inflammatory cytokines were evaluated using relevant methods, including staining, fluorometry, and ELISA. HMGB1 expression was analyzed through Western blotting. The levels of miR-320, HMGB1, neurological deficits, and cerebral infarction were significantly higher after IR induction. Intracerebral overexpression of miR-320 resulted in substantial neurological deficits, increased infarct volume, elevated levels of 8-isoprostane, NF-kappaBp65, TNF-alpha, IL-1beta, ICAM-1, VCAM-1, and HMGB1 expression. It also promoted the loss of mitochondrial membrane potential and ROS levels while reducing MnSOD and GSH levels. Downregulation of miR-320 and inhibition of HMGB1 activity significantly reversed the outcomes of cerebral IR injury. MiR-320 plays a negative role in regulating cerebral inflammatory/oxidative reactions induced by IR injury by enhancing HMGB1 activity and modulating mitochondrial function.
已有研究表明,微RNA可能在脑缺血再灌注(IR)损伤中发挥作用。本研究旨在通过靶向HMGB1/NF-kappaB轴研究microRNA-320(miR-320)在脑IR损伤中的表达及其在脑线粒体功能、氧化应激和炎症反应中的参与。对 Sprague-Dawley 大鼠进行大脑中动脉闭塞以模拟脑 IR 损伤。采用 qRT-PCR 技术评估 miR-320 在大脑中的表达。采用染色法、荧光测定法和酶联免疫吸附法等相关方法评估神经功能、脑梗塞体积、线粒体功能、氧化应激和炎症细胞因子。通过 Western 印迹分析了 HMGB1 的表达。IR诱导后,miR-320、HMGB1、神经功能缺损和脑梗死的水平显著升高。脑内过表达 miR-320 会导致严重的神经功能缺损、脑梗塞体积增大、8-异前列腺素、NF-kappaBp65、TNF-α、IL-1beta、ICAM-1、VCAM-1 和 HMGB1 表达水平升高。它还会促进线粒体膜电位和 ROS 水平的丧失,同时降低 MnSOD 和 GSH 水平。下调 miR-320 和抑制 HMGB1 的活性可明显逆转脑 IR 损伤的结果。MiR-320通过增强HMGB1活性和调节线粒体功能,在调节红外损伤诱导的脑部炎症/氧化反应中发挥负面作用。
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引用次数: 0
Clinical Efficacy of Blood Ultrafiltration Therapy in Patients with Acute Decompensated Chronic Heart Failure Running Title: Blood Ultrafiltration Therapy for Heart Failure. 血液超滤疗法对急性失代偿期慢性心力衰竭患者的临床疗效 Running Title:血液超滤疗法治疗心力衰竭。
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-12-31
Yan-Wei He, Feng-Qin Wang, Fen-Fang Zhang, Huan-Zhen Chen

In this study, we investigated the clinical effects of blood ultrafiltration therapy in patients with acute decompensated chronic heart failure. We enrolled 78 patients with acute decompensated chronic heart failure who were admitted to a hospital from September 2017 to December 2021, and divided them into two groups based on the digital randomization method. The FQ-16 heart failure ultrafiltration dehydrating device blood ultrafiltration therapy was administered to the observation group (39 patients) for 8-16 hours, while the control group (39 patients) received the stepped drug therapy. Echocardiography was used to assess the changes in cardiac function of the patients in both groups before and after treatment. The changes in urine volume, N-terminal pro-B-type natriuretic peptide (NT-proBNP), plasma renin, and serum creatinine levels were measured before and after the treatment to compare the overall response rate of the patients in both groups. The differences in left ventricular end-systolic dimension and left ventricular end-diastolic dimension and the ejection fraction between the groups before treatment were not statistically significant (P > 0.05), however, the left ventricular end-diastolic dimension in the observation group was significantly lower and the ejection fraction was significantly higher (P < 0.05) compared with that before treatment; the urine volume, N-terminal pro-B-type natriuretic peptide (NT-proBNP), plasma renin, and serum creatinine were significantly improved in both groups after treatment compared with that before treatment. All indexes in the observation group were better than those in the control group (P < 0.05), 74.36%. The overall response rate of the observation group was 94.87%, x2 = 4.843 and the difference between groups was statistically significant (P < 0.05). Blood ultrafiltration therapy for patients with acute decompensated chronic heart failure can improve their cardiac and renal functions, reduce NT-proBNP, reduce volume load, and enhance efficacy while ensuring high safety.

在这项研究中,我们探讨了血液超滤疗法对急性失代偿慢性心力衰竭患者的临床效果。我们选取了2017年9月至2021年12月某医院收治的78例急性失代偿慢性心力衰竭患者,根据数字随机法将其分为两组。观察组(39例)给予FQ-16心衰超滤脱水装置血液超滤治疗8-16小时,对照组(39例)接受阶梯药物治疗。采用超声心动图评估两组患者治疗前后心脏功能的变化。通过测量治疗前后尿量、N-末端前 B 型钠尿肽(NT-proBNP)、血浆肾素和血清肌酐水平的变化,比较两组患者的总体反应率。与治疗前相比,两组患者的左室收缩末期尺寸、左室舒张末期尺寸和射血分数差异无统计学意义(P > 0.05),但观察组患者的左室舒张末期尺寸明显降低,射血分数明显升高(P < 0.05);两组治疗后的尿量、N末端前B型钠尿肽(NT-proBNP)、血浆肾素、血清肌酐均较治疗前有明显改善。观察组的各项指标均优于对照组(P<0.05),达 74.36%。观察组的总反应率为 94.87%,x2 = 4.843,组间差异有统计学意义(P < 0.05)。对急性失代偿期慢性心力衰竭患者进行血液超滤治疗,可改善患者的心肾功能,降低NT-proBNP,减轻容量负荷,在保证较高安全性的同时提高疗效。
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引用次数: 0
Modulation of Melatonin Receptors Regulates Reproductive Physiology: The Impact of Agomelatine on the Estrus Cycle, Gestation, Offspring, and Uterine Contractions in Rats. 调节褪黑激素受体可调节生殖生理:阿戈美拉汀对大鼠发情周期、妊娠、后代和子宫收缩的影响
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-12-31
E Kacar, F Tan, S Sahinturk, G Zorlu, I Serhatlioglu, O Bulmus, Z Ercan, H Kelestimur

Agomelatine is a pharmaceutical compound that functions as an agonist for melatonin receptors, with a particular affinity for the MT1 and MT2 receptor subtypes. Its mode of action is integral to the regulation of diverse physiological processes, encompassing the orchestration of circadian rhythms, sleep-wake cycles, and mood modulation. In the present study, we delve into the intricate interplay between agomelatine and the modulation of estrus cycles, gestation periods, offspring numbers, and uterine contractions, shedding light on their collective impact on reproductive physiology. Both in vivo and in vitro experiments were performed. Wistar Albino rats, divided into four groups: two non-pregnant groups (D1 and D2) and two pregnant groups (G1 and G2). The D1 and G1 groups served as control groups, while the D2 and G2 groups received chronic agomelatine administration (10 mg/kg). Uterine contractions were assessed in vitro using myometrial strips. Luzindole, a melatonin receptor antagonist, was employed to investigate the pathway mediating agomelatine's effects on uterine contractions. In in vivo studies, chronic agomelatine administration extended the diestrus phase (p<0.05) in non-pregnant rats, prolonged the gestational period (p<0.01), and increased the fetal count (p<0.01) in pregnant rats. Additionally, agomelatine reduced plasma oxytocin and prostoglandin-E levels (p<0.01) during pregnancy. In vitro experiments showed that agomelatine dose-dependently inhibited spontaneous and oxytocin-induced myometrial contractions. Luzindole (2 µM) reverse the agomelatine-induced inhibition of myometrial contractions. These findings suggest that agomelatine holds the potential to modulate diverse reproductive parameters during the gestational period, influencing estrus cycling, gestational progression, offspring development, and the orchestration of uterine contractions.

阿戈美拉汀是一种药物化合物,可作为褪黑激素受体的激动剂,对 MT1 和 MT2 受体亚型具有特殊的亲和力。它的作用模式与多种生理过程的调节密不可分,包括昼夜节律的协调、睡眠-觉醒周期和情绪调节。在本研究中,我们深入探讨了阿戈美拉汀与发情周期、妊娠期、后代数量和子宫收缩调节之间错综复杂的相互作用,揭示了它们对生殖生理的共同影响。实验同时进行了体内和体外实验。Wistar Albino 大鼠分为四组:两组非妊娠组(D1 和 D2)和两组妊娠组(G1 和 G2)。D1 和 G1 组为对照组,D2 和 G2 组长期服用阿戈美拉汀(10 毫克/千克)。使用子宫肌层条在体外评估子宫收缩情况。褪黑激素受体拮抗剂卢吲哚(Luzindole)被用来研究阿戈美拉汀对子宫收缩影响的介导途径。在体内研究中,长期服用阿戈美拉汀可延长发情期(p
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引用次数: 0
Comparison of Pulmonary and Extrapulmonary Models of Sepsis-Associated Acute Lung Injury. 脓毒症相关急性肺损伤的肺部和肺外模型比较
IF 2.1 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-12-31
G Zhou, D Xie, R Fan, Z Yang, J Du, S Mai, L Xie, Q Wang, T Mai, Y Han, F Lai

To compare different rat models of sepsis at different time points, based on pulmonary or extrapulmonary injury mechanisms, to identify a model which is more stable and reproducible to cause sepsis-associated acute lung injury (ALI). Adult male Sprague-Dawley rats were subjected to (1) cecal ligation and puncture (CLP) with single (CLP1 group) or two repeated through-and-through punctures (CLP2 group); (2) tail vein injection with lipopolysaccharide (LPS) of 10mg/kg (IV-LPS10 group) or 20 mg/kg (IV-LPS20 group); (3) intratracheal instillation with LPS of 10mg/kg (IT-LPS10 group) or 20mg/kg (IT-LPS20 group). Each of the model groups had a sham group. 7-day survival rates of each group were observed (n=15 for each group). Moreover, three time points were set for additional experimental studying in each model group: 4 hours, 24 hours and 48 hours after modeling (every time point, n=8 for each group). Rats were sacrificed to collect BALF and lung tissue samples at different time points for detection of IL-6, TNF-alpha, total protein concentration in BALF and MPO activity, HMGB1 protein expression in lung tissues, as well as the histopathological changes of lung tissues. More than 50 % of the rats died within 7 days in each model group, except for the IT-LPS10 group. In contrast, the mortality rates in the two IV-LPS groups as well as the IT-LPS20 group were significantly higher than that in IT-LPS10 group. Rats received LPS by intratracheal instillation exhibited evident histopathological changes and inflammatory exudation in the lung, but there was no evidence of lung injury in CLP and IV-LPS groups. Rat model of intratracheal instillation with LPS proved to be a more stable and reproducible animal model to cause sepsis-associated ALI than the extrapulmonary models of sepsis.

根据肺部或肺外损伤机制,比较不同时间点的脓毒症大鼠模型,以确定一种更稳定、可重复的引起脓毒症相关急性肺损伤(ALI)的模型。成年雄性 Sprague-Dawley 大鼠分别接受:(1)盲肠结扎和穿刺(CLP),单次(CLP1 组)或两次重复穿刺(CLP2 组);(2)尾静脉注射 10 毫克/千克(IV-LPS10 组)或 20 毫克/千克(IV-LPS20 组)的脂多糖(LPS);(3)气管内灌注 10 毫克/千克(IT-LPS10 组)或 20 毫克/千克(IT-LPS20 组)的 LPS。每个模型组都有一个假组。观察各组的 7 天存活率(每组 n=15)。此外,每个模型组还设置了三个时间点进行额外的实验研究:建模后 4 小时、24 小时和 48 小时(每个时间点,每组 n=8 只)。大鼠在不同的时间点被处死,采集BALF和肺组织样本,用于检测IL-6、TNF-α、BALF中总蛋白浓度和MPO活性、肺组织中HMGB1蛋白表达以及肺组织的组织病理学变化。除 IT-LPS10 组外,各模型组均有 50%以上的大鼠在 7 天内死亡。相比之下,两个静脉注射 LPS 组和 IT-LPS20 组的死亡率明显高于 IT-LPS10 组。气管内灌注 LPS 的大鼠肺部表现出明显的组织病理学变化和炎性渗出,但 CLP 组和 IV-LPS 组没有肺损伤的证据。事实证明,与肺外脓毒症模型相比,气管内灌注 LPS 的大鼠模型是一种更稳定、可重复的引起脓毒症相关 ALI 的动物模型。
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引用次数: 0
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Physiological research
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