Biomedical Research-tokyo最新文献_第2页

Indoxyl sulfate contributes to colorectal cancer cell proliferation and increased EGFR expression by activating AhR and Akt. 硫酸吲哚酯通过激活 AhR 和 Akt 促进结直肠癌细胞增殖和表皮生长因子受体表达增加。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.57

Yu Ichisaka, Shozo Yano, Kohji Nishimura, Toshimitsu Niwa, Hidehisa Shimizu

{"title":"Indoxyl sulfate contributes to colorectal cancer cell proliferation and increased EGFR expression by activating AhR and Akt.","authors":"Yu Ichisaka, Shozo Yano, Kohji Nishimura, Toshimitsu Niwa, Hidehisa Shimizu","doi":"10.2220/biomedres.45.57","DOIUrl":"10.2220/biomedres.45.57","url":null,"abstract":"Although patients with chronic kidney disease (CKD) have a higher risk of colorectal cancer (CRC) aggravation, the connection between these two diseases is not well understood. Recent studies have shown that both CKD and CRC aggravation are closely related to an increased abundance of indole-producing Fusobacterium nucleatum in the gut. The indole absorbed from the gut is eventually metabolized to indoxyl sulfate in the liver. Since indoxyl sulfate is involved not only in accelerating CKD progression but also in the initiation and development of its associated complications, the present study aimed to clarify whether indoxyl sulfate induces the proliferation of CRC cells. This study found that indoxyl sulfate induced the proliferation of CRC-derived HCT-116 cells by activating the aryl hydrocarbon receptor (AhR) and the proto-oncogene Akt. The AhR antagonist CH223191 and Akt inhibitor MK2206 suppressed indoxyl sulfate-induced proliferation of HCT-116 cells. We also found that indoxyl sulfate upregulated epidermal growth factor receptor (EGFR) expression, which is associated with poor prognosis of CRC, whereas CH223191 and MK2206 repressed EGFR expression. Furthermore, indoxyl sulfate increased the sensitivity of CRC cells to EGF by upregulating EGFR expression. These findings suggest that indoxyl sulfate may be an important link between CKD and CRC aggravation.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 2","pages":"57-66"},"PeriodicalIF":1.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140331524","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

Analgesic effects of linalyl acetate via nociceptive TRPV1 inhibition in mice. 乙酸芳樟酯通过抑制小鼠痛觉 TRPV1 产生镇痛效果。

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.217

Miho Hashimoto, Kenji Takahashi, Toshio Ohta

{"title":"Analgesic effects of linalyl acetate via nociceptive TRPV1 inhibition in mice.","authors":"Miho Hashimoto, Kenji Takahashi, Toshio Ohta","doi":"10.2220/biomedres.45.217","DOIUrl":"https://doi.org/10.2220/biomedres.45.217","url":null,"abstract":"Transient receptor potential vanilloid 1 (TRPV1) is primarily expressed in sensory neurons and functions as a nociceptive channel. TRPV1 is activated by capsaicin, acidic pH, and noxious heat. Compounds inhibiting TRPV1 have been explored to develop analgesic drugs. In this study, the effect of linalyl acetate (LA), a lavender essential oil component that exerts analgesic effects, on TRPV1 was investigated by measuring intracellular Ca2+ concentration ([Ca2+]i) and whole-cell membrane currents. The analgesic effects of LA on TRPV1-mediated pain were also examined. LA inhibited [Ca2+]i responses to capsaicin, acidic pH, and heat in mouse sensory neurons. Unlike the transient LA-inhibition on capsaicin- and heat-responses, its inhibition on acid-responses persisted even after the LA removal. In TRPV1-expressing HEK293 cells, LA reversibly suppressed [Ca2+]i responses to capsaicin and heat, but persistently inhibited those to acids. Similarly, LA reversibly attenuated current responses to capsaicin but durably suppressed those to acids. LA sustainingly inhibited the responses to spermine, an endogenous TRPV1 agonist, and reduced pain-related behaviors induced by spermine and noxious heat. These results indicate that LA inhibits TRPV1 in a mode-independent manner, with long-lasting inhibition of acid-induced TRPV1 activation. These inhibitory actions of LA on TRPV1 may be related to its analgesic effects.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 6","pages":"217-230"},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708944","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

Serotonin reuptake inhibitor suppresses the activation of human platelets by a combination of thrombopoietin and collagen through inhibition of Rac and Rho/Rho-kinase. 血清素再摄取抑制剂通过抑制 Rac 和 Rho/Rho-激酶，抑制血小板在血小板生成素和胶原蛋白联合作用下的活化。

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.231

Haruhiko Tokuda, Takamitsu Hori, Takashi Onuma, Yukiko Enomoto, Tomoaki Doi, Rie Matsushima-Nishiwaki, Shinobu Yamaguchi, Kumiko Tanabe, Takuya Omura, Shinji Ogura, Toru Iwama, Hiroki Iida, Osamu Kozawa

{"title":"Serotonin reuptake inhibitor suppresses the activation of human platelets by a combination of thrombopoietin and collagen through inhibition of Rac and Rho/Rho-kinase.","authors":"Haruhiko Tokuda, Takamitsu Hori, Takashi Onuma, Yukiko Enomoto, Tomoaki Doi, Rie Matsushima-Nishiwaki, Shinobu Yamaguchi, Kumiko Tanabe, Takuya Omura, Shinji Ogura, Toru Iwama, Hiroki Iida, Osamu Kozawa","doi":"10.2220/biomedres.45.231","DOIUrl":"https://doi.org/10.2220/biomedres.45.231","url":null,"abstract":"Tramadol and duloxetine, reuptake inhibitors of serotonin and noradrenaline, are widely used analgesics. Cytoplasmic serotonin in human platelets reportedly regulates the activity of low-molecular-weight GTP-binding proteins via serotonylation, leading to the modulation of platelet functions. We recently showed that the combination of thrombopoietin and collagen in the low doses synergistically induces human platelet activation via Rac and Rho/Rho-kinase. In the present study, we investigated the effects of tramadol and duloxetine on the synergistic effect, and the mechanism. Tramadol reduced the platelet aggregation and the release of PDGF-AB by the combination of thrombopoietin and collagen in the low doses. The aggregation and the release were also inhibited by duloxetine. Not reboxetine, a specific inhibitor of noradrenaline transporter, but fluvoxamine and sertraline, specific inhibitors of serotonin transporter suppressed the aggregation and the release. Tramadol, duloxetine, fluvoxamine and sertraline but not reboxetine attenuated the levels of GTP-Rac and GTP-Rho, and phospho-cofilin induced by the combination. Taken together, our results strongly suggest that tramadol and duloxetine, not as noradrenaline reuptake inhibitor but as serotonin reuptake inhibitor, suppress the activation of Rac and Rho/Rho-kinase elicited by the combination of subthreshold thrombopoietin and collagen, leading to the attenuation of human platelet activation.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 6","pages":"231-241"},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708929","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

Linalyl acetate exerts analgesic effects by inhibiting nociceptive TRPA1 in mice. 乙酸芳樟酯通过抑制小鼠的痛觉 TRPA1 发挥镇痛作用。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.125

Miho Hashimoto, Kenji Takahashi, Toshihiro Unno, Toshio Ohta

{"title":"Linalyl acetate exerts analgesic effects by inhibiting nociceptive TRPA1 in mice.","authors":"Miho Hashimoto, Kenji Takahashi, Toshihiro Unno, Toshio Ohta","doi":"10.2220/biomedres.45.125","DOIUrl":"10.2220/biomedres.45.125","url":null,"abstract":"Clary sage essential oil (CSEO) is utilized in perfumery, aromatherapy, and skincare. Linalyl acetate (LA), a primary component of CSEO, possesses sedative, anxiolytic, and analgesic properties. However, the mechanism of its analgesic action is not clearly understood. Transient receptor potential ankyrin 1 (TRPA1) channel, a non-selective cation channel, is mainly expressed in sensory neurons and serves as a sensor of various irritants. In this study, we investigated the effects of LA on TRPA1 channel using heterologous expression system and isolated sensory neurons. To detect channel activity, we employed Ca2+ imaging and the whole-cell patch-clamp technique. The analgesic action of LA was measured in a pain-related behavioral mouse model. In cells that heterologously expressed TRPA1, LA diminished [Ca2+]i and current responses to allylisothiocyanate (AITC) and carvacrol: exogenous TRPA1 agonists, and the inhibitory effects were more pronounced for the former than for the latter. Moreover, LA suppressed [Ca2+] i and current responses to PGJ2: an endogenous TRPA1 agonist. Similar inhibitory actions were observed in native TRPA1 channels expressed in mouse sensory neurons. Furthermore, LA diminished PGJ2-induced nociceptive behaviors in mice. These findings suggest that analgesic effects of LA exert through inhibition of nociceptive TRPA1, making it a potential candidate for novel analgesic development.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 3","pages":"125-133"},"PeriodicalIF":1.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261397","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

Modulation of myocardial injury in polymicrobial sepsis: The dual role of interleukin-13 in cardiac inflammation and stress. 调节多微生物败血症的心肌损伤：白细胞介素-13 在心脏炎症和应激中的双重作用。

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.243

Tsuyoshi Suzuki, Natsuo Yamamoto, Rie Zenda, Hideki Yamamoto, Kazuaki Arai, Ken Iseki

{"title":"Modulation of myocardial injury in polymicrobial sepsis: The dual role of interleukin-13 in cardiac inflammation and stress.","authors":"Tsuyoshi Suzuki, Natsuo Yamamoto, Rie Zenda, Hideki Yamamoto, Kazuaki Arai, Ken Iseki","doi":"10.2220/biomedres.45.243","DOIUrl":"https://doi.org/10.2220/biomedres.45.243","url":null,"abstract":"Polymicrobial sepsis is associated with a poor prognosis due to severe type-1 innate inflammation triggered by immune cells, such as dendritic cells and macrophages. This immune response frequently leads to damage in the heart. Although interleukin (IL)-13 is thought to play a protective role in organ inflammation, its function in polymicrobial sepsis remains unclear. We aimed to investigate the role of IL-13 in modulating myocardial injury during cecal ligation and puncture (CLP)-induced sepsis using a murine model. Cardiac troponin I (cTnI), a biomarker for myocardial damage, was measured in both IL-13-deficient (KO) and wild type (WT) mice subjected to CLP. Contrary to the conventional view of IL-13 as a protective cytokine, IL-13-competent mice exhibited significantly higher serum cTnI levels than IL-13-deficient mice, indicating exacerbated myocardial injury. Elevated cardiac tumor necrosis factor-alpha (TNF-α) levels and IL-1β in WT CLP mice corroborated this finding, suggesting IL-13's role in enhancing the inflammatory response. In vitro assays with bone marrow-derived dendritic cells (BMDCs) stimulated with lipopolysaccharide and Group A Streptococcus revealed a dose-dependent suppression of TNF-α and IL-6 production by recombinant IL-13. These findings indicate a complex role of IL-13 in sepsis, modulating inflammation but potentially increasing myocardial stress.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 6","pages":"243-251"},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708908","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

Quercetin protects human coronary artery endothelial cells against hypoxia/reoxygenation-induced mitochondrial apoptosis via the Nrf2/HO-1 axis. 槲皮素通过Nrf2/HO-1轴保护人冠状动脉内皮细胞免受缺氧/复氧诱导的线粒体凋亡。

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.197

Jiejin Song, Shuang Li, Boyong Zhang, Jiao Wu, Aiqin Zhong

{"title":"Quercetin protects human coronary artery endothelial cells against hypoxia/reoxygenation-induced mitochondrial apoptosis via the Nrf2/HO-1 axis.","authors":"Jiejin Song, Shuang Li, Boyong Zhang, Jiao Wu, Aiqin Zhong","doi":"10.2220/biomedres.45.197","DOIUrl":"10.2220/biomedres.45.197","url":null,"abstract":"Our study explored the therapeutic effect and the mechanism of quercetin against hypoxia/reoxygenation (H/R)-induced injury in human coronary artery endothelial cells (CAECs). Quercetin was selected as a potential component for the BuShenKangShuaiPian formula (BSKSP) treatment via the Network pharmacology analysis. Cell viability and reactive oxygen species (ROS) production were measured by CCK8 assay and immunofluorescence, respectively. The expression of Bax, Bcl-2, Cle-caspase-3, cytochrome c (Cyt-C), NF-E2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) protein was quantified by western blotting. The superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) activity, mtDNA copy number, and ATP production were measured via corresponding kits. Quercetin was selected from the BSKSP for its high degree value (Degree value: 22). Besides, quercetin protected CAECs against H/R-induced cytotoxicity and apoptosis. The H/R-induced increased ROS level, ATP production, Cyt-C release, and decreased mtDNA copy number were removed by the quercetin. Moreover, quercetin upregulated the Nrf2/ HO-1 axis, SOD, and CAT activity, and downregulated MDA levels in H/R treated CAECs, while knockdown Nrf2 reversed the protection of quercetin against H/R-induced oxidative stress, mitochondrial damage, and apoptosis. Quercetin protects CAECs against H/R-induced mitochondrial apoptosis via the Nrf2/HO-1 axis, which innovatively suggests the therapeutic potential of quercetin for coronary heart disease (CHD) treatment.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 5","pages":"197-207"},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380008","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

Epigenetic modification of histone acetylation in the sensorimotor cortex after intracerebral hemorrhage. 脑出血后感觉运动皮层组蛋白乙酰化的表观遗传修饰

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.1

Taichi Nishio, Takahiro Inoue, Yasuyuki Takamatsu, Taiga Mishima, Hana Takamura, Kiho Soma, Yuki Kondo, Misato Okamura, Ryo Ikegami, Hiroshi Maejima

{"title":"Epigenetic modification of histone acetylation in the sensorimotor cortex after intracerebral hemorrhage.","authors":"Taichi Nishio, Takahiro Inoue, Yasuyuki Takamatsu, Taiga Mishima, Hana Takamura, Kiho Soma, Yuki Kondo, Misato Okamura, Ryo Ikegami, Hiroshi Maejima","doi":"10.2220/biomedres.45.1","DOIUrl":"10.2220/biomedres.45.1","url":null,"abstract":"Epigenetic regulation is involved in post-stroke neuroplasticity. We investigated the effects of intracerebral hemorrhage (ICH) on histone acetylation and gene expression related to neuronal plasticity in the bilateral sensorimotor cortices, which may affect post-stroke sensorimotor function. Wistar rats were randomly divided into the SHAM and ICH groups. We performed ICH surgery stereotaxically based on the microinjection of a collagenase solution in the ICH group. Foot fault and cylinder tests were performed to evaluate motor functions at 4-time points, including pre-ICH surgery. The amount of acetyl histones and the mRNA expression of neurotrophic factors crucial to neuroplasticity in the bilateral sensorimotor cortices were analyzed approximately 2 weeks after ICH surgery. Sensorimotor functions of the ICH group were inferior to those of the SHAM group during 2 weeks post-ICH. ICH increased the acetylation of histone H3 and H4 over the sham level in the ipsilateral and contralateral cortices. ICH increased the mRNA expression of IGF-1, but decreased the expression of BDNF compared with the sham level in the ipsilateral cortex. The present study suggests that histone acetylation levels are enhanced in bilateral sensorimotor cortices after ICH, presenting an altered epigenetic platform for gene expressions related to neuronal plasticity.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 1","pages":"1-11"},"PeriodicalIF":1.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139701813","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

Effects of inactivity and exercise intervention on brain-derived neurotrophic factor in mice: Comparison of kinetics in serum, skeletal muscle, and brain. 不运动和运动干预对小鼠脑源性神经营养因子的影响：血清、骨骼肌和大脑中的动力学比较。

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.163

Azusa Miki, Masahiro Aihara, Hikaru Kawaguchi, Noboru Hirose, Hiroki Hagiwara

{"title":"Effects of inactivity and exercise intervention on brain-derived neurotrophic factor in mice: Comparison of kinetics in serum, skeletal muscle, and brain.","authors":"Azusa Miki, Masahiro Aihara, Hikaru Kawaguchi, Noboru Hirose, Hiroki Hagiwara","doi":"10.2220/biomedres.45.163","DOIUrl":"10.2220/biomedres.45.163","url":null,"abstract":"Exercise training increases brain-derived neurotrophic factor (BDNF) expression and improves cognitive function. However, the dynamics of BDNF during inactivity and the effects of exercise intervention on BDNF levels have rarely been examined. Therefore, we aimed to examine changes in serum, skeletal muscle, and brain BDNF levels under these conditions. Mice were divided into control (Co), cast immobilization (CI), reloading (RL), and exercise (Ex) groups. Muscle atrophy was induced by cast immobilization for 2 weeks in the CI, RL, and Ex groups. After cast removal, the RL and Ex groups underwent regrounding and treadmill exercise, respectively, for 2 weeks. Serum, skeletal muscle, and brain BDNF levels showed a similar decreasing trend in the CI group, recovery in the RL group, and a further increase in the Ex group compared with those in the Co group. This indicates that BDNF levels change in parallel with the degree of activity. However, the magnitude of variation differed among the tissues in the order of serum > skeletal muscle > brain tissue. These results suggest that different mechanisms in different tissues regulate BDNF expression. BDNF could potentially act as an objective measure of the impact of both inactivity and exercise-based interventions.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 4","pages":"163-172"},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619325","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

Inhibition of skeletal muscle differentiation by calciprotein particles in human primary myoblasts. 钙蛋白颗粒对人类原发性肌母细胞骨骼肌分化的抑制作用

IF 1.3 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.173

Shohei Kohno, Eisuke Uno, Kazuto Goishi, Davood Kharaghani, Kenta Uchibe, Ryuji Terayama

引用次数: 0

Using hemoglobin vesicles to treat operative hemorrhagic shock after pneu- monectomy in dog models: an experimental study. 在狗模型中使用血红蛋白囊治疗气囊切除术后的手术失血性休克：一项实验研究。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2024-01-01 DOI: 10.2220/biomedres.45.91

Kei Nakano, Mitsutomo Kohno, Hiroto Onozawa, Ryo Hashimoto, Kana Oiwa, Ryota Masuda, Masatoshi Yamaguchi, Tai Hato, Masazumi Watanabe, Hirohisa Horinouchi, Hiromi Sakai, Koichi Kobayashi, Masayuki Iwazaki

{"title":"Using hemoglobin vesicles to treat operative hemorrhagic shock after pneu- monectomy in dog models: an experimental study.","authors":"Kei Nakano, Mitsutomo Kohno, Hiroto Onozawa, Ryo Hashimoto, Kana Oiwa, Ryota Masuda, Masatoshi Yamaguchi, Tai Hato, Masazumi Watanabe, Hirohisa Horinouchi, Hiromi Sakai, Koichi Kobayashi, Masayuki Iwazaki","doi":"10.2220/biomedres.45.91","DOIUrl":"10.2220/biomedres.45.91","url":null,"abstract":"Hemoglobin vesicles (HbVs), considered as red blood cell substitutes, are liposomes encapsulating purified hemoglobin, with a phospholipid bilayer membrane (diameter: 250 nm; P50, 28 Torr). In this study, we aimed to investigate HbV function during hemorrhagic shock in lung resection and analyze the details of oxygen delivery. Left pneumonectomy was performed in dogs under mechanical ventilation, followed by rapid exsanguination of approximately 30% of the total circulating blood volume, which led to shock, reducing the mean arterial pressure (MAP) by approximately 60% of baseline. Subsequently, either 5% human serum albumin (HSA) or HbVs suspended in 5% HSA were infused for resuscitation. The MAP only recovered to 75% of baseline after HSA administration, but fully recovered (100%) after HbV administration, with significant differences between the groups (P < 0.005). Oxygen delivery was restored in the HbV group and was significantly higher than that in the HSA group (P < 0.0001). The infusion of HbVs dispersed in a 5% HSA solution compensated for the rapid loss of approximately 30% of the total circulating blood volume in a dog pneumonectomy model, even with impaired lung function. Thus, HbVs can be used for resuscitation from hemorrhagic shock during thoracic surgery.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"45 2","pages":"91-101"},"PeriodicalIF":1.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140331526","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