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Prazosin Potentiates Mast Cell-Stabilizing Property of Adrenaline 哌唑嗪能增强肾上腺素的肥大细胞稳定特性
Q1 Medicine Pub Date : 2024-05-09 DOI: 10.33594/000000703
Background/Aims: Adrenaline quickly inhibits the release of histamine from mast cells. Besides β2-adrenergic receptors, several in vitro studies also indicate the involvement of α-adrenergic receptors in the process of exocytosis. Since exocytosis in mast cells can be detected electrophysiologically by the changes in the membrane capacitance (Cm), its continuous monitoring in the presence of drugs would determine their mast cell-stabilizing properties. Methods: Employing the whole-cell patch-clamp technique in rat peritoneal mast cells, we examined the effects of adrenaline on the degranulation of mast cells and the increase in the Cm during exocytosis. We also examined the degranulation of mast cells in the presence or absence of α-adrenergic receptor agonists or antagonists. Results: Adrenaline dose-dependently suppressed the GTP-γ-S-induced increase in the Cm and inhibited the degranulation from mast cells, which was almost completely erased in the presence of butoxamine, a β2-adrenergic receptor antagonist. Among α-adrenergic receptor agonists or antagonists, high dose prazosin, a selective α1-adrenergic receptor antagonist, significantly reduced the ratio of degranulating mast cells and suppressed the increase in the Cm. Conclusion: This study provided electrophysiological evidence for the first time that adrenaline dose-dependently inhibited the process of exocytosis, confirming its usefulness as a potent mast cell-stabilizer. The pharmacological blockade of α1-adrenergic receptor by prazosin synergistically potentiated such mast cell-stabilizing property of adrenaline, which is primarily mediated by β2-adrenergic receptors.
背景/目的:肾上腺素能迅速抑制肥大细胞释放组胺。除β2-肾上腺素能受体外,一些体外研究也表明α-肾上腺素能受体参与了外泌过程。由于肥大细胞的外泌作用可通过膜电容(Cm)的变化进行电生理检测,因此在药物存在的情况下对其进行连续监测可确定其稳定肥大细胞的特性。方法:我们在大鼠腹膜肥大细胞中采用了全细胞贴片钳技术,研究了肾上腺素对肥大细胞脱颗粒和外排过程中 Cm 增加的影响。我们还研究了在α肾上腺素能受体激动剂或拮抗剂存在或不存在的情况下肥大细胞脱颗粒的情况。结果显示肾上腺素剂量依赖性地抑制了 GTP-γ-S 诱导的 Cm 升高,并抑制了肥大细胞的脱颗粒,而在β2-肾上腺素能受体拮抗剂丁氧胺的存在下,这种抑制作用几乎完全消失。在α-肾上腺素能受体激动剂或拮抗剂中,大剂量哌唑嗪(一种选择性α1-肾上腺素能受体拮抗剂)能显著降低脱颗粒肥大细胞的比例,并抑制 Cm 的增加。结论本研究首次提供了肾上腺素剂量依赖性抑制外渗过程的电生理学证据,证实了肾上腺素是一种有效的肥大细胞稳定剂。哌唑嗪对α1-肾上腺素能受体的药理阻断协同增强了肾上腺素的这种肥大细胞稳定特性,而这种特性主要是由β2-肾上腺素能受体介导的。
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引用次数: 0
Significant Association of Candidate Genes (AGTR1 and TGF-Β1) Polymorphism with Diabetic Nephropathy in Diabetes Mellitus Type 2 Patients 候选基因(AGTR1 和 TGF-Β1)多态性与 2 型糖尿病患者糖尿病肾病的显著关系
Q1 Medicine Pub Date : 2024-05-06 DOI: 10.33594/000000702
Madeeha Ihsan, Najeeb Ullah Khan
Background/Aims: Diabetic nephropathy (DN) is one of the complications of diabetes mellitus (DM). This study aimed to investigate the association between genetic polymorphisms, specifically AGTR1 (rs5186) and TGF-β1 (rs1800470), and the risk of developing Diabetic nephropathy (DN) in type 2 diabetes mellitus patients, compared to those without DN and healthy controls. Methods: A case-control study was conducted on 165 diabetic patients (59 with diabetic nephropathy (DN) and 54 without DN (DM)), and 52 healthy controls (HC). The genotyping was done using amplification refractory mutation system method (ARMS-PCR). Age, gender, and duration of diabetes were matched across groups. Clinical parameters including FBS, RBS, HbA1C, creatinine, urea, SBP, DBP, total cholesterol, triglycerides, LDL, and BMI were assessed. Results: Diabetic patients with nephropathy exhibited significantly higher levels of clinical parameters compared to those without nephropathy and healthy controls. The risk allele of AGTR1 , C (p <0.0001), and risk allele containing genotypes AC (p <0.0001) and CC (p - 0.0010) were significantly higher in DN patients compared to DM and HC groups. Similarly, the TGF-β1 risk allele C (p - 0.0001), and corresponding genotypes TC (p - 0.0038) and CC (p - 0.0027) were significantly associated with increased risk of diabetic nephropathy compared to DM and HC groups. Conclusion: The data showed significant association of AGTR1 (rs5186) and TGF-β1 (rs1800470) polymorphism with an increased risk of diabetic nephropathy in type 2 diabetes mellitus patients. More investigation will be required to disseminate the results, while increasing the samples size and using whole genome sequencing.
背景/目的:糖尿病肾病(DN)是糖尿病(DM)的并发症之一。本研究旨在调查基因多态性(特别是 AGTR1 (rs5186) 和 TGF-β1 (rs1800470))与 2 型糖尿病患者和无糖尿病肾病患者及健康对照组的糖尿病肾病(DN)发病风险之间的关系。研究方法对 165 名糖尿病患者(59 名糖尿病肾病患者(DN)和 54 名非糖尿病肾病患者(DM))和 52 名健康对照者(HC)进行了病例对照研究。基因分型采用扩增难治性突变系统方法(ARMS-PCR)进行。各组的年龄、性别和糖尿病病程均匹配。临床参数包括 FBS、RBS、HbA1C、肌酐、尿素、SBP、DBP、总胆固醇、甘油三酯、低密度脂蛋白和体重指数。结果与无肾病患者和健康对照组相比,糖尿病肾病患者的临床参数水平明显更高。与 DM 组和 HC 组相比,DN 患者中 AGTR1 的风险等位基因 C(p <0.0001)和风险等位基因含基因型 AC(p <0.0001)和 CC(p - 0.0010)明显较高。同样,与 DM 组和 HC 组相比,TGF-β1 危险等位基因 C(p - 0.0001)以及相应的基因型 TC(p - 0.0038)和 CC(p - 0.0027)与糖尿病肾病风险的增加明显相关。结论数据显示,AGTR1(rs5186)和TGF-β1(rs1800470)多态性与2型糖尿病患者糖尿病肾病风险增加有明显关联。要推广这些结果,还需要进行更多的调查,同时扩大样本量并使用全基因组测序技术。
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引用次数: 0
Retraction. 撤回。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000698
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引用次数: 0
Erratum. 勘误。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000695
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引用次数: 0
Retraction. 撤回。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000697
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引用次数: 0
Erratum. 勘误。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000694
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引用次数: 0
Erratum. 勘误。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000696
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引用次数: 0
Retraction. 撤回。
Q1 Medicine Pub Date : 2024-04-30 DOI: 10.33594/000000699
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引用次数: 0
Acid-Sensitive Outwardly Rectifying Cl- Current in OV2944 Mouse Ovarian Cancer Cells. OV2944 小鼠卵巢癌细胞中对酸敏感的向外整流 Cl- 电流
Q1 Medicine Pub Date : 2024-04-20 DOI: 10.33594/000000692
Hajime Hirasawa, Kayo Aoba, Naofumi Miwa

Background/aims: Extracellular acidic conditions impair cellular activities; however, some cancer cells drive cellular signaling to adapt to the acidic environment. It remains unclear how ovarian cancer cells sense changes in extracellular pH. This study was aimed at characterizing acid-inducible currents in an ovarian cancer cell line and evaluating the involvement of these currents in cell viability.

Methods: The biophysical and pharmacological properties of membrane currents in OV2944, a mouse ovarian cancer cell line, were studied using the whole-cell configuration of the patch-clamp technique. Viability of this cell type in acidic medium was evaluated using the MTT assay.

Results: OV2944 had significant acid-sensitive outwardly rectifying (ASOR) Cl- currents at a pH50 of 5.3. The ASOR current was blocked by pregnenolone sulfate (PS), a steroid ion channel modulator that blocks the ASOR channel as one of its targets. The viability of the cells was reduced after exposure to an acidic medium (pH 5.3) but was slightly restored upon PS administration.

Conclusion: These results offer first evidence for the presence of ASOR Cl- channel in ovarian cancer cells and indicate its involvement in cell viability under acidic environment.

背景/目的:细胞外的酸性条件会损害细胞的活动;然而,一些癌细胞会驱动细胞信号来适应酸性环境。目前仍不清楚卵巢癌细胞如何感知细胞外 pH 值的变化。本研究旨在描述卵巢癌细胞系中酸诱导电流的特征,并评估这些电流参与细胞存活的情况:方法:采用全细胞配置的膜片钳技术研究了小鼠卵巢癌细胞系 OV2944 中膜电流的生物物理和药理学特性。使用 MTT 试验评估了该细胞类型在酸性培养基中的活力:结果:在 pH50 为 5.3 时,OV2944 有明显的酸敏感外向整流(ASOR)Cl- 电流。硫酸孕烯醇酮(PS)可阻断 ASOR 电流,硫酸孕烯醇酮是一种甾体离子通道调节剂,其靶点之一是阻断 ASOR 通道。细胞暴露于酸性培养基(pH 值为 5.3)后活力降低,但在施用 PS 后活力略有恢复:这些结果首次证明了卵巢癌细胞中存在 ASOR Cl- 通道,并表明它参与了细胞在酸性环境下的存活。
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引用次数: 0
Pancreas Β-Cells in Type 1 and Type 2 Diabetes: Cell Death, Oxidative Stress and Immune Regulation. Recently Appearing Changes in Diabetes Consequences. 1 型和 2 型糖尿病患者的胰腺 Β 细胞:细胞死亡、氧化应激和免疫调节。糖尿病后果中最近出现的变化。
Q1 Medicine Pub Date : 2024-04-17 DOI: 10.33594/000000690
Elena G Novoselova, Sergey M Lunin, Maxim O Khrenov, Olga V Glushkova, Tatyana V Novoselova, Svetlana B Parfenyuk

Diabetes mellitus type 1 (T1D) and type 2 (T2D) develop due to dysfunction of the Langerhans islet β-cells in the pancreas, and this dysfunction is mediated by oxidative, endoplasmic reticulum (ER), and mitochondrial stresses. Although the two types of diabetes are significantly different, β-cell failure and death play a key role in the pathogenesis of both diseases, resulting in hyperglycemia due to a reduced ability to produce insulin. In T1D, β-cell apoptosis is the main event leading to hyperglycemia, while in T2D, insulin resistance results in an inability to meet insulin requirements. It has been suggested that autophagy promotes β-cell survival by delaying apoptosis and providing adaptive responses to mitigate the detrimental effects of ER stress and DNA damage, which is directly related to oxidative stress. As people with diabetes are now living longer, they are more susceptible to a different set of complications. There has been a diversification in causes of death, whereby a larger proportion of deaths among individuals with diabetes is attributable to nonvascular conditions; on the other hand, the proportion of cancer-related deaths has remained stable or even increased in some countries. Due to the increasing cases of both T1D and T2D, these diseases become even more socially significant. Hence, we believe that search for any opportunities for control of this disease is an overwhelmingly important target for the modern science. We focus on two differences that are characteristic of the development of diabetes's last periods. One of them shows that all-cause death rates have declined in several diabetes populations, driven in part by large declines in vascular disease mortality but large increases in oncological diseases. Another hypothesis is that some T2D medications could be repurposed to control glycemia in patients with T1D.

1 型糖尿病(T1D)和 2 型糖尿病(T2D)的发病原因是胰腺中的朗格汉斯胰岛β细胞功能失调,而这种功能失调是由氧化、内质网(ER)和线粒体压力介导的。虽然这两种类型的糖尿病有很大不同,但β细胞的衰竭和死亡在这两种疾病的发病机制中都起着关键作用,由于产生胰岛素的能力降低,从而导致高血糖。在 T1D 中,β 细胞凋亡是导致高血糖的主要原因,而在 T2D 中,胰岛素抵抗导致无法满足胰岛素需求。有研究认为,自噬可延缓细胞凋亡,提供适应性反应以减轻 ER 应激和 DNA 损伤(与氧化应激直接相关)的有害影响,从而促进 β 细胞存活。随着糖尿病患者寿命的延长,他们更容易出现一系列不同的并发症。糖尿病患者的死因呈现多样化趋势,非血管性疾病导致的死亡占糖尿病患者死亡的较大比例;另一方面,在一些国家,与癌症相关的死亡比例保持稳定,甚至有所增加。由于 T1D 和 T2D 的病例不断增加,这些疾病的社会意义更加重大。因此,我们认为,寻找控制这种疾病的任何机会都是现代科学的一个极其重要的目标。我们重点关注糖尿病最后发展时期的两个特征性差异。其中之一表明,在一些糖尿病人群中,全因死亡率有所下降,部分原因是血管疾病死亡率大幅下降,但肿瘤疾病死亡率却大幅上升。另一个假设是,一些 T2D 药物可以重新用于控制 T1D 患者的血糖。
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Cellular Physiology and Biochemistry
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