首页 > 最新文献

Pharmacology最新文献

英文 中文
Eleclazine Suppresses Ventricular Fibrillation in Failing Rabbit Hearts with Ischemia- Reperfusion Injury Undergoing Therapeutic Hypothermia. 榄香烯嗪能抑制治疗性低温下缺血再灌注损伤衰竭兔心的室颤
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-10-28 DOI: 10.1159/000542292
Hui-Ling Lee, Po-Cheng Chang, Hung-Ta Wo, Hao-Tien Liu, Ming-Shien Wen, Chung-Chuan Chou

Introduction: Eleclazine is a highly selective late sodium current inhibitor, possibly effective in reducing ventricular fibrillation (VF) in heart failure (HF) with ischemia-reperfusion (IR) injury. The electrophysiological effects of eleclazine at therapeutic hypothermia (TH) are unknown. We investigated the effects of eleclazine in suppressing VF in failing rabbit hearts with IR injury undergoing TH.

Method: HF was induced by right ventricular pacing. An IR model was created using coronary artery ligation for 60 min, followed by reperfusion for 30 min. Hearts were excised and Langendorff-perfused for optical mapping and electrophysiological studies. Electrophysiological studies were repeated after TH (33 oC) for 30 min or eleclazine (1 μM) infusion for 20 min.

Results: In failing IR-injured hearts, eleclazine reduced action potential duration (APD) dispersion and accelerated intracellular Ca2+ uptake to suppress arrhythmogenic alternans, but also exacerbated rate-dependent conduction slowing, resulting in neutral effects on VF inducibility at normothermia. TH increased VF severity. Eleclazine after TH ameliorated TH-induced APD dispersion and further depressed conduction to reduce VF inducibility and severity. TH after eleclazine also slowed conduction to a greater extent to reduce VF inducibility and severity by extrastimulus pacing. In control IR-injured hearts, eleclazine increased VF severity by dynamic pacing at normothermia, which was counteracted by TH.

Conclusions: Eleclazine does not prevent VF at normothermia, but reduces VF inducibility and severity by extrastimulus pacing at TH in isolated failing hearts with regional IR injury.

简介榄香烯是一种高选择性晚期钠离子电流抑制剂,可有效减少缺血再灌注(IR)损伤的心力衰竭(HF)患者的心室颤动(VF)。目前尚不清楚治疗性低温(TH)时依利拉嗪的电生理效应。我们研究了榄香烯嗪抑制IR损伤衰竭兔心在治疗性低温下VF的作用:方法:通过右心室起搏诱导高房颤。方法:通过右心室起搏诱导 HF,使用冠状动脉结扎 60 分钟,然后再灌注 30 分钟,创建 IR 模型。切除心脏并进行朗根多夫灌注,以进行光学绘图和电生理研究。在输注TH(33 oC)30分钟或eleclazine(1 μM)20分钟后重复电生理研究:结果:在红外损伤的衰竭心脏中,榄香烯嗪降低了动作电位持续时间(APD)的弥散性,加速了细胞内Ca2+的摄取,从而抑制了心律失常的交替,但同时也加剧了速率依赖性传导减慢,导致在正常体温下对VF诱导性的影响呈中性。TH 增加了室颤的严重程度。TH 后的利血平可改善 TH 诱导的 APD 弥散,并进一步抑制传导,从而降低室颤的诱发率和严重程度。使用依利卡嗪后,TH 还能在更大程度上减慢传导,从而通过刺激外起搏降低室颤的诱发率和严重程度。在红外损伤的对照心脏中,依来卡嗪增加了常温下动态起搏的室颤严重程度,而TH则抵消了这一作用:结论:在区域性红外损伤的离体衰竭心脏中,榄香烯嗪不能阻止常温下的室颤,但能降低TH下刺激外起搏的室颤诱发率和严重程度。
{"title":"Eleclazine Suppresses Ventricular Fibrillation in Failing Rabbit Hearts with Ischemia- Reperfusion Injury Undergoing Therapeutic Hypothermia.","authors":"Hui-Ling Lee, Po-Cheng Chang, Hung-Ta Wo, Hao-Tien Liu, Ming-Shien Wen, Chung-Chuan Chou","doi":"10.1159/000542292","DOIUrl":"https://doi.org/10.1159/000542292","url":null,"abstract":"<p><strong>Introduction: </strong>Eleclazine is a highly selective late sodium current inhibitor, possibly effective in reducing ventricular fibrillation (VF) in heart failure (HF) with ischemia-reperfusion (IR) injury. The electrophysiological effects of eleclazine at therapeutic hypothermia (TH) are unknown. We investigated the effects of eleclazine in suppressing VF in failing rabbit hearts with IR injury undergoing TH.</p><p><strong>Method: </strong>HF was induced by right ventricular pacing. An IR model was created using coronary artery ligation for 60 min, followed by reperfusion for 30 min. Hearts were excised and Langendorff-perfused for optical mapping and electrophysiological studies. Electrophysiological studies were repeated after TH (33 oC) for 30 min or eleclazine (1 μM) infusion for 20 min.</p><p><strong>Results: </strong>In failing IR-injured hearts, eleclazine reduced action potential duration (APD) dispersion and accelerated intracellular Ca2+ uptake to suppress arrhythmogenic alternans, but also exacerbated rate-dependent conduction slowing, resulting in neutral effects on VF inducibility at normothermia. TH increased VF severity. Eleclazine after TH ameliorated TH-induced APD dispersion and further depressed conduction to reduce VF inducibility and severity. TH after eleclazine also slowed conduction to a greater extent to reduce VF inducibility and severity by extrastimulus pacing. In control IR-injured hearts, eleclazine increased VF severity by dynamic pacing at normothermia, which was counteracted by TH.</p><p><strong>Conclusions: </strong>Eleclazine does not prevent VF at normothermia, but reduces VF inducibility and severity by extrastimulus pacing at TH in isolated failing hearts with regional IR injury.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522754","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
UCF101 Rescues against Diabetes-Evoked Cardiac Remodeling and Contractile Anomalies through AMPK-Mediated Induction of Mitophagy. UCF101 可通过 AMPK 介导的丝裂吞噬作用防止糖尿病诱发的心脏重塑和收缩异常。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-10-16 DOI: 10.1159/000541569
Zhiqiang Zhuang, Yuxi Zhu, Jun Tao, Yandong Liu, Jie Lin, Chunjie Yang, Chule Dong, Xing Qin, Qun Li, Russel J Reiter, Guizhen Wang, Zhaohui Pei, Jun Ren

Background: Diabetes mellitus is known to provoke devastating anomalies in myocardial structure and function while effective therapeutic regimen is still lacking. The selective protease inhibitor UCF101 (5-[5-(2-nitrophenyl) furfuryliodine]-1,3-diphenyl-2-thiobarbituric acid) has been shown to fend off ischemic heart injury although its impact on diabetic cardiomyopathy remains elusive.

Method: Our present work was conducted to examine the effect of UCF101 on experimental diabetes-evoked cardiac geometric and functional abnormalities as well as mechanism involved. Adult mice were made diabetic using streptozotocin (STZ) while receiving UCF101 (7.15 mg/kg, i.p.) for 6 consecutive days.

Result: STZ evidently evoked cardiac hypertrophy, interstitial fibrosis, mitochondrial ultrastructural damage, oxidative stress, dampened autophagy (LC3B, Beclin1, elevated p62), mitophagy (FUNDC1 and Parkin with elevated TOM20), increased left ventricular (LV) end systolic diameter, dampened fractional shortening, ejection fraction, cardiomyocyte shortening capacity, velocities of shortening/relengthening, and rise in intracellular Ca2+ in conjunction with elongated diastole and intracellular Ca2+ removal, the responses were overtly reconciled by UCF101 with little effect from UCF101 itself. Levels of cell injury markers Omi/HtrA2, TNFα, and stress signaling (JNK, ERK, p38) were overtly enhanced along with compromised phosphorylation of cellular fuel AMPK (Thr172) and cell survival molecule GSK3β, as well as downregulated SERCA2a and elevated phospholamban, the effect was reversed by UCF101 (except for SERCA2a). AMPK knockout, pharmacological inhibition, mitophagy inhibitor liensinine and parkin knockout nullified UCF101-offered cardioprotection in diabetes. UCF101 reversed STZ-induced upregulation in the AMPK degrading enzymes PP2A and PP2C.

Conclusion: These findings denote that UCF101 rescues diabetes-instigated alterations in cardiac structure and contraction, likely through AMPK-mediated regulation of mitophagy.

背景:众所周知,糖尿病会导致心肌结构和功能发生破坏性异常,但目前仍缺乏有效的治疗方案。选择性蛋白酶抑制剂 UCF101(5-[5-(2-硝基苯基)呋喃碘]-1,3-二苯基-2-硫代巴比妥酸)已被证明可防止缺血性心脏损伤,但其对糖尿病心肌病的影响仍难以捉摸:本研究旨在探讨 UCF101 对糖尿病诱发的心脏几何和功能异常的影响及其机制。用链脲佐菌素(STZ)使成年小鼠患糖尿病,同时连续 6 天接受 UCF101(7.15 mg/kg,静注):结果:STZ 明显诱发心脏肥大、间质纤维化、线粒体超微结构损伤、氧化应激、自噬(LC3B、Beclin1、p62 升高)、有丝分裂(FUNDC1 和 Parkin 以及 TOM20 升高)受阻、左心室收缩末期直径增大、射血分数缩短受阻、心肌细胞体积减小、射血分数降低、在舒张期延长和细胞内 Ca2+ 清除的同时,UCF101 还能明显调和这些反应,而 UCF101 本身几乎没有影响。细胞损伤标志物 Omi/HtrA2、TNFα 和应激信号转导(JNK、ERK、p38)的水平明显升高,细胞燃料 AMPK(Thr172)和细胞存活分子 GSK3β 的磷酸化受到影响,SERCA2a 下调,磷脂兰班升高,UCF101 逆转了这些影响(SERCA2a 除外)。AMPK基因敲除、药物抑制、有丝分裂抑制剂莲心宁和parkin基因敲除使UCF101对糖尿病患者心脏的保护作用无效。UCF101逆转了STZ诱导的AMPK降解酶PP2A和PP2C的上调:这些研究结果表明,UCF101可能通过AMPK介导的有丝分裂调节,挽救糖尿病诱发的心脏结构和收缩的改变。
{"title":"UCF101 Rescues against Diabetes-Evoked Cardiac Remodeling and Contractile Anomalies through AMPK-Mediated Induction of Mitophagy.","authors":"Zhiqiang Zhuang, Yuxi Zhu, Jun Tao, Yandong Liu, Jie Lin, Chunjie Yang, Chule Dong, Xing Qin, Qun Li, Russel J Reiter, Guizhen Wang, Zhaohui Pei, Jun Ren","doi":"10.1159/000541569","DOIUrl":"https://doi.org/10.1159/000541569","url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus is known to provoke devastating anomalies in myocardial structure and function while effective therapeutic regimen is still lacking. The selective protease inhibitor UCF101 (5-[5-(2-nitrophenyl) furfuryliodine]-1,3-diphenyl-2-thiobarbituric acid) has been shown to fend off ischemic heart injury although its impact on diabetic cardiomyopathy remains elusive.</p><p><strong>Method: </strong>Our present work was conducted to examine the effect of UCF101 on experimental diabetes-evoked cardiac geometric and functional abnormalities as well as mechanism involved. Adult mice were made diabetic using streptozotocin (STZ) while receiving UCF101 (7.15 mg/kg, i.p.) for 6 consecutive days.</p><p><strong>Result: </strong>STZ evidently evoked cardiac hypertrophy, interstitial fibrosis, mitochondrial ultrastructural damage, oxidative stress, dampened autophagy (LC3B, Beclin1, elevated p62), mitophagy (FUNDC1 and Parkin with elevated TOM20), increased left ventricular (LV) end systolic diameter, dampened fractional shortening, ejection fraction, cardiomyocyte shortening capacity, velocities of shortening/relengthening, and rise in intracellular Ca2+ in conjunction with elongated diastole and intracellular Ca2+ removal, the responses were overtly reconciled by UCF101 with little effect from UCF101 itself. Levels of cell injury markers Omi/HtrA2, TNFα, and stress signaling (JNK, ERK, p38) were overtly enhanced along with compromised phosphorylation of cellular fuel AMPK (Thr172) and cell survival molecule GSK3β, as well as downregulated SERCA2a and elevated phospholamban, the effect was reversed by UCF101 (except for SERCA2a). AMPK knockout, pharmacological inhibition, mitophagy inhibitor liensinine and parkin knockout nullified UCF101-offered cardioprotection in diabetes. UCF101 reversed STZ-induced upregulation in the AMPK degrading enzymes PP2A and PP2C.</p><p><strong>Conclusion: </strong>These findings denote that UCF101 rescues diabetes-instigated alterations in cardiac structure and contraction, likely through AMPK-mediated regulation of mitophagy.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472878","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
Tanshinone IIA inhibits H2O2-induced ferroptosis in melanocytes through activating Nrf2 signaling pathway. 丹参酮 IIA 可通过激活 Nrf2 信号通路抑制 H2O2 诱导的黑色素细胞铁突变。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-10-16 DOI: 10.1159/000541177
Xiaosha Li, Shiyang Tang, Haizhen Wang, Xin Li

Introduction: Melanocyte ferroptosis has been proven to contribute to the development of vitiligo. Tanshinone IIA (TSA), a Chinese herbal extract, has been shown to inhibit vitiligo progression. Whether TSA regulates ferroptosis in melanocytes remains unclear.

Methods: Hydrogen peroxide (H2O2) was used to induce melanocytes to stimulate vitiligo cell model in vitro. Cell proliferation was examined by 5-ethynyl-2'-deoxyuridine assay. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), glutathione peroxidase (GSH) and iron (Fe2+) were detected by corresponding commercial kit. The protein levels of ferroptosis-related markers and Nrf2 pathway-related markers were examined using western blot and immunofluorescence staining. Cell viability and cytotoxicity were analyzed using cell counting kit 8 assay and lactate dehydrogenase (LDH) detection. Mitochondrial morphology was examined using a transmission electron microscope.

Results: After H2O2 treatment, melanocyte proliferation was reduced, while oxidative stress and ferroptosis were enhanced. TSA treatment could inhibit ferroptosis in H2O2-induced melanocytes. Besides, TSA could activate Nrf2 pathway and promote Nrf2 nuclear translocation, and Nrf2 specific inhibitor (ML385) also reversed the inhibitory effect of TSA on H2O2-induced melanocyte ferroptosis.

Conclusion: Our data showed that TSA alleviated H2O2-induced melanocyte ferroptosis via activating Nrf2 pathway.

简介黑色素细胞铁蛋白沉着已被证实是导致白癜风发病的原因之一。丹参酮 IIA(TSA)是一种中药提取物,已被证明可抑制白癜风的发展。方法:用过氧化氢(H2O2)在体外诱导黑色素细胞刺激白癜风细胞模型。细胞增殖采用 5-乙炔基-2'-脱氧尿苷检测法。丙二醛(MDA)、活性氧(ROS)、谷胱甘肽过氧化物酶(GSH)和铁(Fe2+)的水平由相应的商业试剂盒检测。采用 Western 印迹和免疫荧光染色法检测铁突变相关标记物和 Nrf2 通路相关标记物的蛋白水平。使用细胞计数试剂盒 8 和乳酸脱氢酶(LDH)检测分析细胞活力和细胞毒性。使用透射电子显微镜检查线粒体形态:结果:H2O2 处理后,黑色素细胞增殖减少,氧化应激和铁凋亡增强。TSA 可抑制 H2O2 诱导的黑色素细胞的铁突变。此外,TSA能激活Nrf2通路并促进Nrf2核转位,Nrf2特异性抑制剂(ML385)也能逆转TSA对H2O2诱导的黑色素细胞铁突变的抑制作用:结论:我们的研究数据表明,TSA通过激活Nrf2通路缓解了H2O2诱导的黑色素细胞铁突变。
{"title":"Tanshinone IIA inhibits H2O2-induced ferroptosis in melanocytes through activating Nrf2 signaling pathway.","authors":"Xiaosha Li, Shiyang Tang, Haizhen Wang, Xin Li","doi":"10.1159/000541177","DOIUrl":"https://doi.org/10.1159/000541177","url":null,"abstract":"<p><strong>Introduction: </strong>Melanocyte ferroptosis has been proven to contribute to the development of vitiligo. Tanshinone IIA (TSA), a Chinese herbal extract, has been shown to inhibit vitiligo progression. Whether TSA regulates ferroptosis in melanocytes remains unclear.</p><p><strong>Methods: </strong>Hydrogen peroxide (H2O2) was used to induce melanocytes to stimulate vitiligo cell model in vitro. Cell proliferation was examined by 5-ethynyl-2'-deoxyuridine assay. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), glutathione peroxidase (GSH) and iron (Fe2+) were detected by corresponding commercial kit. The protein levels of ferroptosis-related markers and Nrf2 pathway-related markers were examined using western blot and immunofluorescence staining. Cell viability and cytotoxicity were analyzed using cell counting kit 8 assay and lactate dehydrogenase (LDH) detection. Mitochondrial morphology was examined using a transmission electron microscope.</p><p><strong>Results: </strong>After H2O2 treatment, melanocyte proliferation was reduced, while oxidative stress and ferroptosis were enhanced. TSA treatment could inhibit ferroptosis in H2O2-induced melanocytes. Besides, TSA could activate Nrf2 pathway and promote Nrf2 nuclear translocation, and Nrf2 specific inhibitor (ML385) also reversed the inhibitory effect of TSA on H2O2-induced melanocyte ferroptosis.</p><p><strong>Conclusion: </strong>Our data showed that TSA alleviated H2O2-induced melanocyte ferroptosis via activating Nrf2 pathway.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472877","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
Rat Model of Menopausal/Andropausal Hypertension with Different Sensitivities to Non-Genomic Antihypertensive Responses of Female and Male Sex Steroids. 更年期/雄激素性高血压大鼠模型对雌性和雄性性激素非基因组降压反应的敏感性不同。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-10-15 DOI: 10.1159/000542007
Mercedes Perusquía, Nieves Herrera

Introduction: Hypertension is prevalent in older women and men, but the impact of sex differences is unclear.

Methods: Blood pressure (BP) was evaluated weekly for 15 weeks using tail-cuff plethysmography in intact or gonadectomized female and male rats. Similarly, gonadectomized rats were subcutaneously treated daily for 15 weeks with estradiol in females or testosterone in males. Treatment with estrogen in males and androgen in females for BP was also examined. The non-genomic antihypertensive potency and efficacy of different sex steroids were determined; catheters were implanted in the carotid artery of hypertensive rats for BP recording with bolus injections in the jugular vein at cumulative doses (1 × 10-7-1 × 10-4M kg-1 min-1) of dehydroepiandrosterone (DHEA), estradiol, testosterone, or 5β-dihydrotestosterone (5β-DHT).

Results: Data showed a time-dependent increase in BP after gonadectomy in female and male rats until hypertension values were reached. Males are more sensitive to the development of hypertension than females. The increases in BP in females and males were completely prevented by estradiol or testosterone, respectively. Testosterone completely prevented hypertension in females, whereas estradiol only partially in males. Antihypertensive potencies in conscious hypertensive rats were DHEA = 5β-DHT = testosterone >> estradiol, in females and DHEA = 5β-DHT >> testosterone >> estradiol in males. The efficacy was DHEA = 5β-DHT = testosterone >> estradiol in females and 5β-DHT = DHEA >> testosterone >> estradiol in males.

Conclusion: Gonadectomized males developed hypertension faster than females, suggesting that androgen deficiency plays an important role in BP reduction. Antihypertensive responses of steroids are structure-dependent; estradiol demonstrated the lowest potency, whereas 5β-DHT was a potent antihypertensive without estrogenic and androgenic actions, suggesting it is as a therapeutic candidate for controlling hypertension in both sexes.

导言:高血压在老年女性和男性中都很普遍,但性别差异的影响尚不清楚:方法:在连续 15 周的时间里,使用尾袖褶式压力计对完整或性腺切除的雌性和雄性大鼠的血压(BP)进行每周一次的评估。同样,对性腺切除的雌性大鼠或雄性大鼠每天皮下注射雌二醇或睾酮,连续治疗 15 周。此外,还对雄性大鼠和雌性大鼠使用雌激素和雄激素治疗血压进行了研究。测定了不同性类固醇的非基因组降压效力和疗效;在高血压大鼠的颈动脉植入导管,在颈静脉注射累积剂量(1x10-7-1x10-4 M kg-1 min-1)的脱氢表雄酮(DHEA)、雌二醇、睾酮或 5β- 二氢睾酮(5β-DHT),记录血压。结果:数据显示,雌性和雄性大鼠在性腺切除后,血压的升高与时间有关,直至达到高血压值。雄性对高血压的发生比雌性更敏感。雌性和雄性血压的升高分别被雌二醇或睾酮完全阻止。睾酮可完全防止雌性高血压,而雌二醇只能部分防止雄性高血压。在有意识的高血压大鼠中,雌性的抗高血压效力为 DHEA=5β-DHT=testosterone>>estradiol; 雄性的抗高血压效力为 DHEA=5β-DHT>>testosterone>>estradiol.女性的疗效为DHEA=5β-DHT=睾酮>>雌二醇,男性的疗效为5β-DHT=DHEA>>睾酮>>雌二醇:结论:性腺切除的男性比女性患高血压的速度更快,这表明雄激素缺乏在降低血压方面起着重要作用。类固醇的抗高血压反应与结构有关,雌二醇的效力最低,而5β-DHT则是一种强效抗高血压药物,不具有雌激素和雄激素作用,这表明它是控制两性高血压的候选治疗药物。
{"title":"Rat Model of Menopausal/Andropausal Hypertension with Different Sensitivities to Non-Genomic Antihypertensive Responses of Female and Male Sex Steroids.","authors":"Mercedes Perusquía, Nieves Herrera","doi":"10.1159/000542007","DOIUrl":"10.1159/000542007","url":null,"abstract":"<p><strong>Introduction: </strong>Hypertension is prevalent in older women and men, but the impact of sex differences is unclear.</p><p><strong>Methods: </strong>Blood pressure (BP) was evaluated weekly for 15 weeks using tail-cuff plethysmography in intact or gonadectomized female and male rats. Similarly, gonadectomized rats were subcutaneously treated daily for 15 weeks with estradiol in females or testosterone in males. Treatment with estrogen in males and androgen in females for BP was also examined. The non-genomic antihypertensive potency and efficacy of different sex steroids were determined; catheters were implanted in the carotid artery of hypertensive rats for BP recording with bolus injections in the jugular vein at cumulative doses (1 × 10-7-1 × 10-4<sc>M</sc> kg-1 min-1) of dehydroepiandrosterone (DHEA), estradiol, testosterone, or 5β-dihydrotestosterone (5β-DHT).</p><p><strong>Results: </strong>Data showed a time-dependent increase in BP after gonadectomy in female and male rats until hypertension values were reached. Males are more sensitive to the development of hypertension than females. The increases in BP in females and males were completely prevented by estradiol or testosterone, respectively. Testosterone completely prevented hypertension in females, whereas estradiol only partially in males. Antihypertensive potencies in conscious hypertensive rats were DHEA = 5β-DHT = testosterone >> estradiol, in females and DHEA = 5β-DHT >> testosterone >> estradiol in males. The efficacy was DHEA = 5β-DHT = testosterone >> estradiol in females and 5β-DHT = DHEA >> testosterone >> estradiol in males.</p><p><strong>Conclusion: </strong>Gonadectomized males developed hypertension faster than females, suggesting that androgen deficiency plays an important role in BP reduction. Antihypertensive responses of steroids are structure-dependent; estradiol demonstrated the lowest potency, whereas 5β-DHT was a potent antihypertensive without estrogenic and androgenic actions, suggesting it is as a therapeutic candidate for controlling hypertension in both sexes.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472876","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
Erratum. 勘误。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-10-10 DOI: 10.1159/000541793
{"title":"Erratum.","authors":"","doi":"10.1159/000541793","DOIUrl":"10.1159/000541793","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401044","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
Non-Coding RNA Networks in Pulmonary Arterial Hypertension. 肺动脉高压中的非编码 RNA 网络
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-09-27 DOI: 10.1159/000541060
Bing Chen, Yu Xia, Yanjiao Jiang, Zengxian Sun, Yanyan Zhang, Yun Liu

Background: Pulmonary artery hypertension (PAH) is a severe cardiovascular disease marked by a persistent increase in pulmonary artery resistance and pressure, leading to right ventricular strain, hypertrophy, and eventually right heart failure and death. Despite numerous available targeted therapies, the clinical needs for treating PAH remain unmet. Current treatments primarily aim to dilate pulmonary vessels rather than reverse pulmonary vascular remodeling, failing to offer a fundamental solution for PAH. Therefore, developing new therapies for this condition is urgently required.

Summary: Recent research has highlighted the crucial role of non-coding RNAs (ncRNAs) in the occurrence and development of PAH. NcRNAs, such as long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs), and PIWI-interacting RNAs (piRNAs), are a class of transcripts that do not translate proteins but affect various diseases at different levels, including chromatin modification, transcription regulation, post-translational processes.

Key message: The current study delves into recent advancements in understanding how lncRNAs, circRNAs, miRNAs, and piRNAs contribute to the pathogenesis of PAH. This review addresses the existing research challenges and explores the potential of ncRNAs as both biomarkers and therapeutic targets, suggesting that ncRNAs may serve as valuable indicators and treatment options for the disease.

背景:肺动脉高压(PAH)是一种严重的心血管疾病,其特点是肺动脉阻力和压力持续增加,导致右心室劳损、肥大,最终导致右心衰竭和死亡。尽管目前有许多靶向疗法,但治疗 PAH 的临床需求仍未得到满足。目前的治疗方法主要是扩张肺血管,而不是逆转肺血管重塑,无法从根本上解决 PAH 问题。因此,迫切需要开发治疗这种疾病的新疗法:最近的研究强调了非编码 RNA(ncRNA)在 PAH 发生和发展过程中的关键作用。ncRNAs,如长非编码RNAs(lncRNA)、环状RNAs(circRNA)、microRNAs(miRNA)和PIWI-interacting RNAs(piRNA),是一类不翻译蛋白质的转录本,但在不同水平上影响各种疾病,包括染色质修饰、转录调控、翻译后过程等:本研究深入探讨了最近在了解 lncRNA、circRNA、miRNA 和 piRNA 如何促进 PAH 发病机制方面取得的进展。这篇综述探讨了现有的研究挑战,并探索了 ncRNAs 作为生物标志物和治疗靶点的潜力,认为 ncRNAs 可作为该疾病的重要指标和治疗方案。
{"title":"Non-Coding RNA Networks in Pulmonary Arterial Hypertension.","authors":"Bing Chen, Yu Xia, Yanjiao Jiang, Zengxian Sun, Yanyan Zhang, Yun Liu","doi":"10.1159/000541060","DOIUrl":"10.1159/000541060","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary artery hypertension (PAH) is a severe cardiovascular disease marked by a persistent increase in pulmonary artery resistance and pressure, leading to right ventricular strain, hypertrophy, and eventually right heart failure and death. Despite numerous available targeted therapies, the clinical needs for treating PAH remain unmet. Current treatments primarily aim to dilate pulmonary vessels rather than reverse pulmonary vascular remodeling, failing to offer a fundamental solution for PAH. Therefore, developing new therapies for this condition is urgently required.</p><p><strong>Summary: </strong>Recent research has highlighted the crucial role of non-coding RNAs (ncRNAs) in the occurrence and development of PAH. NcRNAs, such as long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs), and PIWI-interacting RNAs (piRNAs), are a class of transcripts that do not translate proteins but affect various diseases at different levels, including chromatin modification, transcription regulation, post-translational processes.</p><p><strong>Key message: </strong>The current study delves into recent advancements in understanding how lncRNAs, circRNAs, miRNAs, and piRNAs contribute to the pathogenesis of PAH. This review addresses the existing research challenges and explores the potential of ncRNAs as both biomarkers and therapeutic targets, suggesting that ncRNAs may serve as valuable indicators and treatment options for the disease.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142352535","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
Additive Inhibition of HERG Channels Expressed in Xenopus Oocytes by Antipsychotic Drugs and Citrus Juice Flavonoid Naringenin. 抗精神病药物和柑橘类黄酮柚皮苷对爪蟾卵母细胞中表达的 HERG 通道的相加抑制作用。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-09-26 DOI: 10.1159/000541005
Keun-Hang Susan Yang, Dmytro Isaev, Murat Oz

Introduction: Citrus juice has been shown to cause QT prolongation in electrocardiograms of healthy volunteers, and naringenin, a major flavonoid found in citrus juice, has been identified as the potent inhibitor of human ether-a-go-go-related gene (HERG) channels as the cause of QT prolongation. Inhibition of HERG channels and prolongation of QT interval by antipsychotic drugs such as haloperidol, chlorpromazine, and clozapine have also been shown. However, naringenin's effect on HERG channel function in conjunction with antipsychotic medications has not been investigated.

Methods: In the present study, we evaluated the effect of combining naringenin with antipsychotics on the function of HERG channels expressed in Xenopus oocytes.

Results: When 30 µm naringenin was added to antipsychotic drugs (1 µm haloperidol, 10 µm chlorpromazine, or 10 µm clozapine), significantly greater HERG inhibition was demonstrated, compared to the inhibition caused by antipsychotic drugs alone. Co-application studies also showed that the magnitudes of inhibitions caused by naringenin + antipsychotics were similar to that predicted by the allotopic interaction model, suggesting that naringenin and antipsychotics bind to the HERG channel at different sites.

Conclusion: The results suggest that there is an additive interaction between antipsychotics and naringenin. Due to the potential for repolarization heterogeneity and a decrease in repolarization reserve, this additive HERG inhibition may increase the risk of arrhythmias.

背景:柑橘汁已被证实会导致健康志愿者的心电图出现 QT 间期延长,而柑橘汁中的主要黄酮类化合物柚皮苷已被确认为导致 QT 间期延长的强效 HERG 通道抑制剂。有报告称,氟哌啶醇、氯丙嗪和氯氮平等几种抗精神病药物也会抑制 HERG 通道,并延长用药患者的 QT 间期。然而,柚皮苷与抗精神病药物对 HERG 通道功能的相互作用尚未得到研究:在本研究中,我们评估了柚皮苷与抗精神病药物联合使用对在爪蟾卵母细胞中表达的 HERG 通道功能的影响:结果:在抗精神病药物(1 µM氟哌啶醇、10 µM氯丙嗪或10 µM氯氮平)中加入30 µM柚皮苷,与单独使用抗精神病药物相比,HERG抑制作用明显增强:结论:研究结果表明,柚皮素与抗精神病药物之间存在相加作用。结论:研究结果表明,柚皮苷与抗精神病药物之间会产生相加作用,这种相加的 HERG 抑制作用会降低再极化储备并可能导致再极化异质性,从而增加心律失常的风险。
{"title":"Additive Inhibition of HERG Channels Expressed in Xenopus Oocytes by Antipsychotic Drugs and Citrus Juice Flavonoid Naringenin.","authors":"Keun-Hang Susan Yang, Dmytro Isaev, Murat Oz","doi":"10.1159/000541005","DOIUrl":"10.1159/000541005","url":null,"abstract":"<p><strong>Introduction: </strong>Citrus juice has been shown to cause QT prolongation in electrocardiograms of healthy volunteers, and naringenin, a major flavonoid found in citrus juice, has been identified as the potent inhibitor of human ether-a-go-go-related gene (HERG) channels as the cause of QT prolongation. Inhibition of HERG channels and prolongation of QT interval by antipsychotic drugs such as haloperidol, chlorpromazine, and clozapine have also been shown. However, naringenin's effect on HERG channel function in conjunction with antipsychotic medications has not been investigated.</p><p><strong>Methods: </strong>In the present study, we evaluated the effect of combining naringenin with antipsychotics on the function of HERG channels expressed in Xenopus oocytes.</p><p><strong>Results: </strong>When 30 µ<sc>m</sc> naringenin was added to antipsychotic drugs (1 µ<sc>m</sc> haloperidol, 10 µ<sc>m</sc> chlorpromazine, or 10 µ<sc>m</sc> clozapine), significantly greater HERG inhibition was demonstrated, compared to the inhibition caused by antipsychotic drugs alone. Co-application studies also showed that the magnitudes of inhibitions caused by naringenin + antipsychotics were similar to that predicted by the allotopic interaction model, suggesting that naringenin and antipsychotics bind to the HERG channel at different sites.</p><p><strong>Conclusion: </strong>The results suggest that there is an additive interaction between antipsychotics and naringenin. Due to the potential for repolarization heterogeneity and a decrease in repolarization reserve, this additive HERG inhibition may increase the risk of arrhythmias.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142352534","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
Expression of Concern. 表达关切。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-09-16 DOI: 10.1159/000541269
{"title":"Expression of Concern.","authors":"","doi":"10.1159/000541269","DOIUrl":"https://doi.org/10.1159/000541269","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142293606","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
Disruption of Lipid Profile, Glucose Metabolism, and Leptin Levels following Citalopram Administration and High-Carbohydrate and High-Cholesterol Diet in Mice. 给小鼠服用西酞普兰并摄入高碳水化合物和高胆固醇饮食后,小鼠的血脂状况、葡萄糖代谢和瘦素水平会受到破坏。
IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-09-05 DOI: 10.1159/000541229
Tomáš Hammer, Hana Kotolová, Jiří Procházka, Michal Karpíšek

Introduction: Depression therapy has been linked to negative effects on energy metabolism, which can be attributed to various factors, including an ongoing inflammatory process commonly seen in metabolic disorders. Unhealthy lifestyle choices of patients and the impact of antidepressants on body weight and lipid and glucose metabolism also contribute to these metabolic side effects. Although not as pronounced as other psychopharmaceuticals, the increasing use of antidepressants raises concerns about their potential impact on public health. The study aimed to evaluate the short- and long-term effects of the antidepressant citalopram and its long-term combination with a special diet on metabolic parameters in mice.

Methods: Animals were randomly divided into 5 groups - control, control + special diet, citalopram (10 mg/kg for 35 days), citalopram + special diet (10 mg/kg for 35 days), and citalopram (10 mg/kg for 7 days). After a described time of administration, animals were anesthetized, blood and fat and liver tissues were collected. Biochemical parameters of lipid metabolism (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides) and glucose were analyzed using spectrophotometry and relevant adipokines and cytokines were evaluated by ELISA.

Results: After a week of application of citalopram, we observed dyslipidemia that persisted even at the end of the 5-week experiment. Furthermore, after 5 weeks of citalopram administration, we observed a significant decrease in body weight gain and decreased leptin levels. Changes in lipid metabolism, higher levels of adipokines leptin and PAI-1 were observed due to the special diet after 5 weeks.

Conclusions: Our research suggests that the effects of citalopram and a diet on the metabolism of mice can be significant, both in the short term (1 week) and in the long term (5 weeks).

导言 抑郁症治疗与对能量代谢的负面影响有关,这可归因于多种因素,包括代谢紊乱中常见的持续炎症过程。患者选择不健康的生活方式以及抗抑郁药物对体重、脂质和葡萄糖代谢的影响也是造成这些代谢副作用的原因。尽管抗抑郁药的使用不像其他精神药物那样明显,但其使用量的增加引起了人们对其对公众健康潜在影响的担忧。本研究旨在评估抗抑郁药西酞普兰及其与特殊饮食长期结合对小鼠代谢参数的短期和长期影响。方法 将动物随机分为 5 组--对照组、对照组+特殊饮食组、西酞普兰组(10 毫克/千克,35 天)、西酞普兰+特殊饮食组(10 毫克/千克,35 天)和西酞普兰组(10 毫克/千克,7 天)。在所述给药时间后,对动物进行麻醉,采集血液、脂肪和肝组织。用分光光度法分析脂质代谢的生化指标(总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、甘油三酯)和葡萄糖,用酶联免疫吸附法评估相关的脂肪因子和细胞因子。结果 在服用西酞普兰一周后,我们观察到血脂异常,甚至在五周实验结束时血脂异常仍然存在。此外,在服用西酞普兰五周后,我们观察到体重增加明显减少,瘦素水平也有所下降。五周后,由于特殊饮食,我们观察到脂质代谢发生了变化,脂肪因子瘦素和 PAI-1 水平升高。结论 我们的研究表明,无论是短期(1 周)还是长期(5 周),西酞普兰和饮食对小鼠新陈代谢的影响都是显著的。
{"title":"Disruption of Lipid Profile, Glucose Metabolism, and Leptin Levels following Citalopram Administration and High-Carbohydrate and High-Cholesterol Diet in Mice.","authors":"Tomáš Hammer, Hana Kotolová, Jiří Procházka, Michal Karpíšek","doi":"10.1159/000541229","DOIUrl":"10.1159/000541229","url":null,"abstract":"<p><strong>Introduction: </strong>Depression therapy has been linked to negative effects on energy metabolism, which can be attributed to various factors, including an ongoing inflammatory process commonly seen in metabolic disorders. Unhealthy lifestyle choices of patients and the impact of antidepressants on body weight and lipid and glucose metabolism also contribute to these metabolic side effects. Although not as pronounced as other psychopharmaceuticals, the increasing use of antidepressants raises concerns about their potential impact on public health. The study aimed to evaluate the short- and long-term effects of the antidepressant citalopram and its long-term combination with a special diet on metabolic parameters in mice.</p><p><strong>Methods: </strong>Animals were randomly divided into 5 groups - control, control + special diet, citalopram (10 mg/kg for 35 days), citalopram + special diet (10 mg/kg for 35 days), and citalopram (10 mg/kg for 7 days). After a described time of administration, animals were anesthetized, blood and fat and liver tissues were collected. Biochemical parameters of lipid metabolism (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides) and glucose were analyzed using spectrophotometry and relevant adipokines and cytokines were evaluated by ELISA.</p><p><strong>Results: </strong>After a week of application of citalopram, we observed dyslipidemia that persisted even at the end of the 5-week experiment. Furthermore, after 5 weeks of citalopram administration, we observed a significant decrease in body weight gain and decreased leptin levels. Changes in lipid metabolism, higher levels of adipokines leptin and PAI-1 were observed due to the special diet after 5 weeks.</p><p><strong>Conclusions: </strong>Our research suggests that the effects of citalopram and a diet on the metabolism of mice can be significant, both in the short term (1 week) and in the long term (5 weeks).</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140851","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 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY Pub Date : 2024-09-03 DOI: 10.1159/000540933
{"title":"Retraction Statement.","authors":"","doi":"10.1159/000540933","DOIUrl":"https://doi.org/10.1159/000540933","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142126391","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
期刊
Pharmacology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1