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Safety of Tigecycline in Patients on Antithrombotic Therapy: A Single-Center Retrospective Study. 替加环素在抗血栓治疗患者中的安全性:一项单中心回顾性研究。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 Epub Date: 2023-09-26 DOI: 10.1159/000532001
Chuwen Lin, Miaoqin Tan, Dongmei Wang, Chunping Gu, Yongming Wu, Shengnan Wang

Introduction: The aims of the study were to investigate the risk factors of tigecycline-induced hypofibrinogenemia and to evaluate the safety of tigecycline with concomitant antithrombotic drugs.

Methods: We performed a retrospective analysis of patients who received tigecycline for more than 3 days between January 2015 and June 2019. Clinical and laboratory data were collected including fibrinogen concertation, tigecycline dose, duration of treatment, disease severity, complete blood count, indicators of infection, liver and renal function. Risk factors of hypofibrinogenemia were analyzed by univariate and multivariate analysis. To evaluate the safety of tigecycline and concomitant antithrombotic drugs, bleeding events were assessed by comparing the decline in hemoglobin and the amount of red blood cell transfusion in patients with antithrombotic drugs and those without.

Results: This study included a total of 68 cases, 20 of which experienced hypofibrinogenemia while receiving tigecycline treatment. Duration of treatment, cefoperazone/sulbactam combination therapy, and fibrinogen levels prior to initiation of tigecycline were risk factors associated with tigecycline-induced hypofibrinogenemia. There were 26 recorded bleeding incidents, 25 of which happened before the start of tigecycline. Antithrombotic and non-antithrombotic patients did not differ in their hemoglobin decline or need for red blood cell transfusions while taking tigecycline.

Conclusion: A longer treatment duration, cefoperazone/sulbactam combination therapy, and a lower level of fibrinogen before tigecycline were associated with an increased risk of tigecycline-induced hypofibrinogenemia. A combination of antithrombotic drugs and tigecycline did not aggravate the bleeding events during tigecycline treatment.

引言:本研究的目的是调查替加环素诱导的低纤维蛋白原血症的危险因素,并评估替加环肽联合抗血栓药物的安全性。方法:我们对2015年1月至2019年6月期间接受替加环素治疗超过3天的患者进行了回顾性分析。收集临床和实验室数据,包括纤维蛋白原浓度、替加环素剂量、治疗时间、疾病严重程度、全血细胞计数、感染指标、肝肾功能。采用单因素和多因素分析法分析低纤维蛋白原血症的危险因素。为了评估替加环素和联合抗血栓药物的安全性,通过比较服用抗血栓药物和未服用抗血栓药的患者血红蛋白和红细胞输注量的下降来评估出血事件。结果:本研究共纳入68例患者,其中20例在接受替加环素治疗时出现低纤维蛋白原血症。治疗持续时间、头孢哌酮/舒巴坦联合治疗和替加环素治疗前纤维蛋白原水平是与替加环肽诱导的低纤维蛋白原血症相关的危险因素。记录在案的出血事件有26起,其中25起发生在替加环素治疗开始前。抗血栓患者和非抗血栓患者在服用替加环素时血红蛋白下降或需要输注红细胞方面没有差异。结论:在替加环素治疗前,较长的治疗时间、头孢哌酮/舒巴坦联合治疗和较低的纤维蛋白原水平与替加环肽诱导的低纤维蛋白原血症的风险增加有关。在替加环素治疗期间,抗血栓药物和替加环肽的联合用药不会加重出血事件。
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引用次数: 0
Metformin's Role in Hyperlactatemia and Lactic Acidosis in ICU Patients: A Systematic Review. 二甲双胍在ICU患者高乳酸血症和乳酸性酸中毒中的作用:一项系统综述。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000528252
Livia Mueller, Michel Moser, Josef Prazak, Daniel G Fuster, Joerg C Schefold, Patrick Zuercher

Introduction: Metformin-treated patients may experience severe hyperlactatemia or lactic acidosis (LA). LA often requires intensive-care-unit (ICU) treatment, and mortality rates are high. Here, we investigate the impact of renal dysfunction and renal replacement therapy (RRT) on the outcomes of critically ill patients with metformin-associated LA (MALA). Furthermore, we assessed associations between mortality and metformin dose, metformin plasma/serum concentrations, lactate level, and arterial pH. Finally, we investigated whether the recommended classification in MALA, metformin-unrelated LA, metformin-induced LA, and LA in metformin therapy appears useful in this regard.

Methods: We performed a retrospective analysis based on a systematic PubMed search for publications on hyperlactatemia/LA in metformin-treated ICU patients from January 1995 to February 2020. Case-level data including demographics and clinical conditions were extracted, and logistic regression analyses were performed.

Results: A total of 92 ICU patients were reported. Two of these patients had no comorbidities interfering with lactate metabolism. In the overall group, arterial pH, lactate levels, and metformin plasma/serum concentrations were similar in survivors versus non-survivors. Ingested daily metformin doses and plasma/serum creatinine levels were significantly higher in survivors versus non-survivors (p = 0.007 vs. p = 0.024, respectively). Higher plasma/serum creatinine levels, higher lactate levels, and lower arterial pH were all associated with patients receiving RRT (all p < 0.05). Overall mortality was 22% (20 out of 92 patients) and did not differ between the RRT and non-RRT groups.

Conclusion: Mortality is high in ICU patients with metformin-associated hyperlactatemia/LA. Unexpectedly, higher ingested metformin dose and plasma/serum creatinine were associated with a better outcome. Survival was similar in patients with or without need for RRT.

二甲双胍治疗的患者可能会出现严重的高乳酸血症或乳酸酸中毒(LA)。洛杉矶通常需要重症监护病房(ICU)治疗,死亡率很高。在这里,我们研究肾功能障碍和肾脏替代治疗(RRT)对二甲双胍相关性LA (MALA)危重患者预后的影响。此外,我们评估了死亡率与二甲双胍剂量、二甲双胍血浆/血清浓度、乳酸水平和动脉ph之间的关系。最后,我们调查了二甲双胍治疗中MALA、二甲双胍无关LA、二甲双胍诱导LA和LA的推荐分类在这方面是否有用。方法:我们基于PubMed系统检索1995年1月至2020年2月二甲双胍治疗的ICU患者高乳酸血症/LA的出版物进行回顾性分析。提取病例级数据,包括人口统计学和临床情况,并进行logistic回归分析。结果:共报告ICU患者92例。其中2例患者没有干扰乳酸代谢的合并症。在整个组中,幸存者与非幸存者的动脉pH值、乳酸水平和二甲双胍血浆/血清浓度相似。幸存者与非幸存者相比,每日摄取的二甲双胍剂量和血浆/血清肌酐水平显著更高(p = 0.007 vs. p = 0.024)。较高的血浆/血清肌酐水平、较高的乳酸水平和较低的动脉pH值均与接受RRT的患者相关(均p < 0.05)。总死亡率为22%(92例患者中有20例),在RRT组和非RRT组之间没有差异。结论:二甲双胍相关性高乳酸血症/LA在ICU患者中死亡率较高。出乎意料的是,较高的二甲双胍摄入剂量和血浆/血清肌酐与较好的结果相关。需要或不需要RRT的患者的生存率相似。
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引用次数: 1
Etomidate Depresses Spontaneous Complex Spikes Activity of Cerebellar Purkinje Cells via Cannabinoid 1 Receptor in vivo in Mice. 依托咪酯在小鼠体内通过大麻素1受体抑制小脑浦肯野细胞的自发复合物尖峰活性。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 Epub Date: 2023-08-22 DOI: 10.1159/000531680
Wen Pan, Chun-Ping Chu, De-Lai Qiu

Introduction: Complex spikes (CSs) activity of cerebellar Purkinje cells plays critical roles in motor coordination and motor learning by transferring information to cerebellar cortex, which is an accessible and useful model for neurophysiological investigation. Etomidate is an ultrashort-acting nonbarbiturate intravenous anesthetic, which inhibits the spontaneous activity of cerebellar Purkinje cells through activation of GABAA and glycine receptors in vivo in mice. However, the effect of etomidate on the spontaneous CSs activity of cerebellar Purkinje cells in living mouse is not clear.

Methods: We here investigated the effects of etomidate on spontaneous CSs activity of cerebellar Purkinje cell in urethane-anesthetized mice by electrophysiology recording technique and pharmacological methods.

Results: Our results showed that cerebellar surface perfusion of etomidate significantly depressed the activity of spontaneous CSs, which exhibited decreases in the number of spikelets and the area under curve (AUC) of the CSs. The etomidate-produced inhibition of CSs activity was persisted in the presence of GABAA and glycine receptors antagonists. However, application of cannabinoid 1 (CB1) receptor antagonist, AM-251, completely blocked the etomidate-induced inhibition of CSs. Furthermore, application of the CB1 receptor agonist, WIN55212-2, induced a decrease of CSs. Moreover, in the presence of a specific protein kinase A (PKA) inhibitor, KT5720, etomidate failed to produce decreases in the spikelets number and the AUC of the spontaneous CSs.

Conclusion: These results indicate that cerebellar surface application of etomidate facilitates CB1 receptor activity resulting in a depression of spontaneous CSs activity of Purkinje cells via PKA signaling pathway in mouse cerebellar cortex. Our present results suggest that the etomidate administration may impair the function of cerebellar cortical neuronal circuitry by inhibition of the climbing fiber - Purkinje cells synaptic transmission through activation of CB1 receptors in vivo in mice.

引言:小脑浦肯野细胞的复杂棘波(CS)活动通过将信息传递到小脑皮层,在运动协调和运动学习中发挥着关键作用,这是一种可获得且有用的神经生理学研究模型。依托咪酯是一种超短效非巴比妥类静脉麻醉药,通过激活小鼠体内GABAA和甘氨酸受体来抑制小脑浦肯野细胞的自发活动。然而,依托咪酯对活体小鼠小脑浦肯野细胞自发CSs活性的影响尚不清楚。方法:采用电生理记录技术和药理学方法研究依托咪酯对氨基甲酸乙酯麻醉小鼠小脑浦肯野细胞自发CSs活性的影响。结果:我们的结果表明,小脑表面灌注依托咪酯显著降低了自发CSs的活性,表现为CSs的小穗数和曲线下面积(AUC)降低。依托咪酯对CS活性的抑制作用在GABAA和甘氨酸受体拮抗剂的存在下持续存在。然而,大麻素1(CB1)受体拮抗剂AM-251的应用完全阻断了依托咪酯诱导的CS的抑制作用。此外,CB1受体激动剂WIN55212-2的应用诱导了CS的减少。此外在特异性蛋白激酶a(PKA)抑制剂KT5720存在下,依托咪酯不能降低自发CSs的小穗数和AUC。我们目前的研究结果表明,依托咪酯给药可能通过激活小鼠体内CB1受体来抑制攀爬纤维-浦肯野细胞的突触传递,从而损害小脑皮层神经元回路的功能。
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引用次数: 0
Canagliflozin Ameliorates Ventricular Remodeling through Apelin/Angiotensin-Converting Enzyme 2 Signaling in Heart Failure with Preserved Ejection Fraction Rats. 卡格列净通过Apelin/血管紧张素转换酶2信号传导改善射血分数保留的心力衰竭大鼠心室重构。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 Epub Date: 2023-08-23 DOI: 10.1159/000533277
Tingting Zhang, Xinyu Wang, Zhongli Wang, Jianlong Zhai, Lili He, Yan Wang, Qingjuan Zuo, Sai Ma, Guorui Zhang, Yifang Guo

Introduction: The aim of this study was to investigate the effect of canagliflozin (CANA) on ventricular remodeling in patients with preserved ejection fraction (HFpEF) heart failure and to further investigate its possible molecular mechanisms.

Methods: A high-salt diet was used to induce the formation of HFpEF model in salt-sensitive rats. The rats were fed with CANA and irbesartan, respectively. The mice were divided into control group, model group, CANA group, irbesartan group, and combined drug group. After 12 weeks of feeding, the rats were evaluated by measuring the relevant indexes and echocardiography for cardiac function. Histological analysis was performed using Masson trichrome staining and immunohistochemical staining. RT-qPCR and Western blot were used to quantify the relevant genes and proteins.

Results: In this study, CANA exhibited diuresis, decreased blood pressure, weight loss, and increased food and water intake. Following a high-salt diet, Dahl salt-sensitive rats developed hypertension followed by left ventricular diastolic dysfunction, myocardial fibrosis, and left ventricular remodeling. Myocardial hypertrophy and fibrosis were reduced, and left ventricular diastolic function and ventricular remodeling improved after CANA treatment. The combination of CANA and irbesartan was superior to monotherapy in reducing blood pressure and improving cardiac insufficiency and left ventricular diastolic dysfunction in rats. CANA improves myocardial fibrosis, left ventricular diastolic dysfunction, and ventricular remodeling by upregulating apelin, activating angiotensin-converting enzyme 2 (ACE2), and increasing ACE2/Ang (1-7)/MASR axis levels.

Conclusion: CANA improves myocardial fibrosis, left ventricular diastolic dysfunction, and ventricular remodeling in HFpEF rats through upregulation of apelin/ACE2 signaling.

引言:本研究旨在探讨卡格列净(CANA)对保留射血分数(HFpEF)心力衰竭患者心室重构的影响,并进一步探讨其可能的分子机制。方法:采用高盐饮食诱导盐敏感大鼠形成HFpEF模型。大鼠分别喂食CANA和厄贝沙坦。将小鼠分为对照组、模型组、CANA组、厄贝沙坦组和联合用药组。喂食12周后,通过测量相关指标和超声心动图对大鼠的心功能进行评估。使用Masson三色染色和免疫组织化学染色进行组织学分析。采用RT-qPCR和蛋白质印迹法对相关基因和蛋白质进行定量。结果:在这项研究中,CANA表现出利尿、降压、减肥以及增加食物和水的摄入。高盐饮食后,达尔盐敏感大鼠出现高血压,随后出现左心室舒张功能障碍、心肌纤维化和左心室重构。CANA治疗后,心肌肥厚和纤维化减轻,左心室舒张功能和心室重构改善。CANA和厄贝沙坦联合用药在降低大鼠血压、改善心功能不全和左心室舒张功能障碍方面优于单药治疗。CANA通过上调apelin、激活血管紧张素转换酶2(ACE2)和增加ACE2/Ang(1-7)/MASR轴水平,改善心肌纤维化、左心室舒张功能障碍和心室重塑。结论:CANA通过上调apelin/ACE2信号传导改善HFpEF大鼠心肌纤维化、左心室舒张功能障碍和心室重构。
{"title":"Canagliflozin Ameliorates Ventricular Remodeling through Apelin/Angiotensin-Converting Enzyme 2 Signaling in Heart Failure with Preserved Ejection Fraction Rats.","authors":"Tingting Zhang,&nbsp;Xinyu Wang,&nbsp;Zhongli Wang,&nbsp;Jianlong Zhai,&nbsp;Lili He,&nbsp;Yan Wang,&nbsp;Qingjuan Zuo,&nbsp;Sai Ma,&nbsp;Guorui Zhang,&nbsp;Yifang Guo","doi":"10.1159/000533277","DOIUrl":"10.1159/000533277","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of this study was to investigate the effect of canagliflozin (CANA) on ventricular remodeling in patients with preserved ejection fraction (HFpEF) heart failure and to further investigate its possible molecular mechanisms.</p><p><strong>Methods: </strong>A high-salt diet was used to induce the formation of HFpEF model in salt-sensitive rats. The rats were fed with CANA and irbesartan, respectively. The mice were divided into control group, model group, CANA group, irbesartan group, and combined drug group. After 12 weeks of feeding, the rats were evaluated by measuring the relevant indexes and echocardiography for cardiac function. Histological analysis was performed using Masson trichrome staining and immunohistochemical staining. RT-qPCR and Western blot were used to quantify the relevant genes and proteins.</p><p><strong>Results: </strong>In this study, CANA exhibited diuresis, decreased blood pressure, weight loss, and increased food and water intake. Following a high-salt diet, Dahl salt-sensitive rats developed hypertension followed by left ventricular diastolic dysfunction, myocardial fibrosis, and left ventricular remodeling. Myocardial hypertrophy and fibrosis were reduced, and left ventricular diastolic function and ventricular remodeling improved after CANA treatment. The combination of CANA and irbesartan was superior to monotherapy in reducing blood pressure and improving cardiac insufficiency and left ventricular diastolic dysfunction in rats. CANA improves myocardial fibrosis, left ventricular diastolic dysfunction, and ventricular remodeling by upregulating apelin, activating angiotensin-converting enzyme 2 (ACE2), and increasing ACE2/Ang (1-7)/MASR axis levels.</p><p><strong>Conclusion: </strong>CANA improves myocardial fibrosis, left ventricular diastolic dysfunction, and ventricular remodeling in HFpEF rats through upregulation of apelin/ACE2 signaling.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"478-491"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10433964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction Statement. 撤回声明。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 Epub Date: 2023-06-22 DOI: 10.1159/000531416
{"title":"Retraction Statement.","authors":"","doi":"10.1159/000531416","DOIUrl":"10.1159/000531416","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"495"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9677287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Research Progress on the Anticancer Molecular Mechanism of Targets Regulating Cell Autophagy. 调控细胞自噬的抗癌靶点分子机制研究进展。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000529279
Ting Zhang, Jia Yu, Sha Cheng, Ya Zhang, Chang-Hua Zhou, Juan Qin, Heng Luo

Background: Autophagy is a lysosome-mediated catabolic process that maintains cell homeostasis and survival. It occurs not only in normal cells such as cardiac muscle cells, neurons, and pancreatic acinar cells but also in various benign and malignant tumors. The abnormal level of intracellular autophagy is closely related to multiple pathophysiological processes, including aging, neurodegeneration, infectious diseases, immune disorders, and cancer. Autophagy mainly plays a dual role in life and death by regulating cell survival, proliferation, and death, thus being involved in the occurrence, development, and treatment of cancer. It is also involved in chemotherapy resistance by a dual role, since it not only promotes the occurrence of drug resistance but also reverses it. Previous findings suggest that the regulation of autophagy can be used as an effective strategy in tumor therapy.

Summary: Recent studies found that small molecules from natural products and their derivatives exert anticancer activity by regulating the level of autophagy in tumor cells.

Key messages: Therefore, this review article describes the mechanism of autophagy, the role of autophagy in normal cells and tumor cells, and the research progress on the anticancer molecular mechanism of targets regulating cell autophagy. The aim is to provide a theoretical basis for developing autophagy inhibitors or activators to improve anticancer efficacy.

背景:自噬是一种溶酶体介导的分解代谢过程,维持细胞稳态和存活。它不仅存在于心肌细胞、神经元、胰腺腺泡细胞等正常细胞中,也存在于各种良恶性肿瘤中。细胞内自噬水平异常与多种病理生理过程密切相关,包括衰老、神经退行性疾病、传染病、免疫紊乱、癌症等。自噬主要通过调节细胞的存活、增殖和死亡,在生命和死亡中起着双重作用,参与了癌症的发生、发展和治疗。它还以双重作用参与化疗耐药,既能促进耐药的发生,又能逆转耐药。以往的研究结果表明,调节自噬可以作为一种有效的肿瘤治疗策略。摘要:近年来的研究发现,天然产物及其衍生物中的小分子通过调节肿瘤细胞的自噬水平来发挥抗癌作用。因此,本文综述了自噬的发生机制,自噬在正常细胞和肿瘤细胞中的作用,以及调控细胞自噬的靶点抗癌分子机制的研究进展。目的是为开发自噬抑制剂或激活剂以提高抗癌效果提供理论依据。
{"title":"Research Progress on the Anticancer Molecular Mechanism of Targets Regulating Cell Autophagy.","authors":"Ting Zhang,&nbsp;Jia Yu,&nbsp;Sha Cheng,&nbsp;Ya Zhang,&nbsp;Chang-Hua Zhou,&nbsp;Juan Qin,&nbsp;Heng Luo","doi":"10.1159/000529279","DOIUrl":"https://doi.org/10.1159/000529279","url":null,"abstract":"<p><strong>Background: </strong>Autophagy is a lysosome-mediated catabolic process that maintains cell homeostasis and survival. It occurs not only in normal cells such as cardiac muscle cells, neurons, and pancreatic acinar cells but also in various benign and malignant tumors. The abnormal level of intracellular autophagy is closely related to multiple pathophysiological processes, including aging, neurodegeneration, infectious diseases, immune disorders, and cancer. Autophagy mainly plays a dual role in life and death by regulating cell survival, proliferation, and death, thus being involved in the occurrence, development, and treatment of cancer. It is also involved in chemotherapy resistance by a dual role, since it not only promotes the occurrence of drug resistance but also reverses it. Previous findings suggest that the regulation of autophagy can be used as an effective strategy in tumor therapy.</p><p><strong>Summary: </strong>Recent studies found that small molecules from natural products and their derivatives exert anticancer activity by regulating the level of autophagy in tumor cells.</p><p><strong>Key messages: </strong>Therefore, this review article describes the mechanism of autophagy, the role of autophagy in normal cells and tumor cells, and the research progress on the anticancer molecular mechanism of targets regulating cell autophagy. The aim is to provide a theoretical basis for developing autophagy inhibitors or activators to improve anticancer efficacy.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":"108 3","pages":"224-237"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9521861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Cardiometabolic Risk Factors in Atorvastatin-Treated Women with Euthyroid Autoimmune Thyroiditis. 阿托伐他汀治疗的甲状腺自身免疫性甲状腺炎妇女的心脏代谢危险因素
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000529242
Robert Krysiak, Karolina Kowalcze, Bogusław Okopień

Introduction: Autoimmune thyroiditis seems to be associated with increased cardiometabolic risk. Statins, the mainstay of cardiovascular risk reduction and prevention, were found to reduce thyroid antibody titers. The aim of this study was to investigate plasma markers of cardiometabolic risk in statin-treated women with thyroid autoimmunity.

Methods: We compared two matched groups of euthyroid women with hypercholesterolemia receiving atorvastatin treatment: subjects with autoimmune (Hashimoto's) thyroiditis (group A, n = 29) and subjects without thyroid pathology (group B, n = 29). Plasma lipids, glucose homeostasis markers, as well as circulating levels of uric acid, high-sensitivity C-reactive protein (hsCRP), fibrinogen, homocysteine, and 25-hydroxyvitamin D were measured before atorvastatin treatment and 6 months later.

Results: At entry, both groups differed in antibody titers, insulin sensitivity, and plasma levels of uric acid, hsCRP, fibrinogen, homocysteine, and 25-hydroxyvitamin D. Atorvastatin-induced reduction in hsCRP and homocysteine, but not in total cholesterol and LDL-cholesterol, was more pronounced in group B than in group A. Only in group B, the drug decreased uric acid and fibrinogen and increased 25-hydroxyvitamin D. In group A, atorvastatin reduced insulin responsiveness.

Conclusion: The obtained results indicate that euthyroid women with Hashimoto's thyroiditis may benefit to a lesser degree from atorvastatin treatment than other populations of women with hypercholesterolemia.

自身免疫性甲状腺炎似乎与心脏代谢风险增加有关。他汀类药物是降低和预防心血管疾病风险的主要药物,可降低甲状腺抗体滴度。本研究的目的是研究他汀类药物治疗的甲状腺自身免疫妇女心脏代谢风险的血浆标志物。方法:我们比较了两组匹配的接受阿托伐他汀治疗的甲状腺功能正常的高胆固醇血症妇女:自身免疫性(桥本)甲状腺炎患者(A组,n = 29)和无甲状腺病理的患者(B组,n = 29)。在阿托伐他汀治疗前和6个月后测量血浆脂质、葡萄糖稳态标志物以及尿酸、高敏c反应蛋白(hsCRP)、纤维蛋白原、同型半胱氨酸和25-羟基维生素D的循环水平。结果:在入组时,两组在抗体滴度、胰岛素敏感性、血浆尿酸、hsCRP、纤维蛋白原、同型半胱氨酸和25-羟基维生素d水平上存在差异。阿托伐他汀诱导的hsCRP和同型半胱氨酸的降低,而不是总胆固醇和低密度脂蛋白胆固醇的降低,在B组比A组更明显。只有在B组,药物降低了尿酸和纤维蛋白原,增加了25-羟基维生素d。结论:获得的结果表明,与其他高胆固醇血症妇女相比,甲状腺功能正常的桥本甲状腺炎妇女从阿托伐他汀治疗中获益的程度较低。
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引用次数: 2
Inhibition of Kv7/M Channel Currents by Fangchinoline. 芳胆碱对Kv7/M通道电流的抑制作用。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000527464
Han Li, DanDan Geng, Rong Zheng, Runmeng Wang, Yaning Li, Yidong Liu, Qingzhong Jia, Fan Zhang

Introduction: Voltage-gated Kv7/M potassium channels play an essential role in the control of membrane potential and neuronal excitability. Fangchinoline, a bisbenzylisoquinoline alkaloid, displays extensive biological activities including antitumor, anti-inflammatory, and antihypertension effects. In this study, we investigated the effects of fangchinoline on Kv7/M channels.

Methods: A perforated whole-cell patch technique was used to record Kv7 currents from HEK293 cells and M-type currents from mouse dorsal root ganglion (DRG) neurons.

Results: Fangchinoline inhibited Kv7.2/Kv7.3 currents in a concentration-dependent manner, with an IC50 of 9.5 ± 1.2 μM. Fangchinoline significantly inhibited Kv7.1, Kv7.2, Kv7.3, Kv7.4, and Kv7.3/Kv7.5 channels without selective effects. Furthermore, fangchinoline significantly slowed the activation of Kv7.1-Kv7.5 channels and inhibited native M-channel currents of DRG neurons.

Conclusion: Taken together, our findings indicate that fangchinoline concentration-dependently inhibited Kv7/M channel currents.

电压门控的Kv7/M钾通道在控制膜电位和神经元兴奋性中起着重要作用。芳喹啉是一种双苄基异喹啉类生物碱,具有抗肿瘤、抗炎、降压等广泛的生物活性。在本研究中,我们研究了防胆碱对Kv7/M通道的影响。方法:采用全细胞穿孔贴片技术记录HEK293细胞的Kv7电流和小鼠背根神经节(DRG)神经元的m型电流。结果:芳胆碱抑制Kv7.2/Kv7.3电流呈浓度依赖性,IC50为9.5±1.2 μM。方胆碱对Kv7.1、Kv7.2、Kv7.3、Kv7.4和Kv7.3/Kv7.5通道的抑制作用无选择性。此外,fangchinoline显著减缓了Kv7.1-Kv7.5通道的激活,抑制了DRG神经元的m通道电流。结论:综上所述,我们的研究结果表明,抗胆碱浓度依赖于抑制Kv7/M通道电流。
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引用次数: 0
Erratum. 勘误表。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000529046
{"title":"Erratum.","authors":"","doi":"10.1159/000529046","DOIUrl":"https://doi.org/10.1159/000529046","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":"108 3","pages":"308"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10235202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Protective Effects and Mechanisms of Flavonoids in Renal Ischemia-Reperfusion Injury. 黄酮类化合物对肾缺血再灌注损伤的保护作用及其机制。
IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2023-01-01 DOI: 10.1159/000527262
Peng Peng, Junrong Zou, Bin Zhong, Guoxi Zhang, Xiaofeng Zou, Tianpeng Xie

Background: Acute kidney injury (AKI) is a common and potentially fatal complication encountered during a variety of kidney surgeries. Renal ischemia/reperfusion (I/R) injury is the predominant mechanism of AKI in this setting. Hence, controlling I/R injury is a key research imperative as it is directly related to the prognosis of patients.

Summary: In the last decade, studies in vitro and in animal models have demonstrated that flavonoids can significantly alleviate I/R-induced AKI through a variety of pathways, including anti-oxidative stress, anti-inflammation, anti-cell death, inhibition of endoplasmic reticulum stress, and alleviation of mitochondrial dysfunction. Based on the extensive role of flavonoids in ischemia-reperfusion injury, the lack of drugs entering the clinic so far is a question worthy of consideration.

Key messages: This review summarizes the available evidence pertaining to the protective effect of flavonoids against renal I/R injury and discusses their potential clinical application in renal I/R injury.

背景:急性肾损伤(AKI)是各种肾脏手术中常见且可能致命的并发症。肾缺血/再灌注(I/R)损伤是AKI的主要机制。因此,控制I/R损伤是当务之急,因为它直接关系到患者的预后。摘要:近十年来,体外和动物模型研究表明,黄酮类化合物可以通过抗氧化应激、抗炎症、抗细胞死亡、抑制内质网应激和减轻线粒体功能障碍等多种途径显著缓解I/ r诱导的AKI。基于黄酮类化合物在缺血再灌注损伤中的广泛作用,目前进入临床的药物缺乏是一个值得思考的问题。本文综述了黄酮类化合物对肾I/R损伤保护作用的现有证据,并讨论了其在肾I/R损伤中的潜在临床应用。
{"title":"Protective Effects and Mechanisms of Flavonoids in Renal Ischemia-Reperfusion Injury.","authors":"Peng Peng,&nbsp;Junrong Zou,&nbsp;Bin Zhong,&nbsp;Guoxi Zhang,&nbsp;Xiaofeng Zou,&nbsp;Tianpeng Xie","doi":"10.1159/000527262","DOIUrl":"https://doi.org/10.1159/000527262","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) is a common and potentially fatal complication encountered during a variety of kidney surgeries. Renal ischemia/reperfusion (I/R) injury is the predominant mechanism of AKI in this setting. Hence, controlling I/R injury is a key research imperative as it is directly related to the prognosis of patients.</p><p><strong>Summary: </strong>In the last decade, studies in vitro and in animal models have demonstrated that flavonoids can significantly alleviate I/R-induced AKI through a variety of pathways, including anti-oxidative stress, anti-inflammation, anti-cell death, inhibition of endoplasmic reticulum stress, and alleviation of mitochondrial dysfunction. Based on the extensive role of flavonoids in ischemia-reperfusion injury, the lack of drugs entering the clinic so far is a question worthy of consideration.</p><p><strong>Key messages: </strong>This review summarizes the available evidence pertaining to the protective effect of flavonoids against renal I/R injury and discusses their potential clinical application in renal I/R injury.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":"108 1","pages":"27-36"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10479607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
期刊
Pharmacology
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