EXPERIMENTAL ANIMALS实验动物
EXPERIMENTAL ANIMALS(英文缩写 EXP ANIM TOKYO),ISSN 1341-1357,eISSN 1881-7122,中文译名:实验动物 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 1.798 | Q2 |
| 2022 | 2.400 | Q1 |
| 2023 | 2.200 | Q1 |
| 2024 | 1.200 | Q2 |
| 2025 | 2.000 | Q1 |
EXPERIMENTAL ANIMALS 最新收录文献
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1. Remimazolam improves survival and attenuates glycocalyx-related injury after hemorrhagic shock in rats.
PMID:日期:2026-09-18Systemic inflammatory activation and endothelial glycocalyx injury contribute to organ dysfunction and poor outcomes after hemorrhagic shock. We investigated whether remimazolam improved survival and attenuated inflammatory activation and glycocalyx-related injury in a rat model of hemorrhagic shock and explored whether these effects were sensitive to flumazenil. Ninety male Sprague-Dawley rats underwent hemorrhagic shock by reducing mean arterial pressure to 40-45 mmHg for 60 minutes, followed by fluid resuscitation. Animals were assigned to five groups: normal saline (Control-S), low-dose remimazolam (LowR, 5 mg/kg), high-dose remimazolam (HighR, 10 mg/kg), high-dose remimazolam with flumazenil (Control-F), and flumazenil alone (Flu). Survival time, serum tumor necrosis factor-α, serum syndecan-1, myocardial glycocalyx thickness, and coverage ratio were evaluated. Survival time differed significantly among the five groups (overall log-rank P=0.00025). Remimazolam was associated with lower serum tumor necrosis factor-α and syndecan-1 levels than those in the control groups. Animal-level TEM analysis showed significant overall group differences in endothelial glycocalyx thickness and coverage ratio, although no adjusted pairwise comparisons reached statistical significance. Remimazolam administration was associated with improved survival, lower tumor necrosis factor-α levels, reduced circulating glycocalyx shedding, and a pattern suggestive of partial structural glycocalyx preservation in this rat model of hemorrhagic shock. Flumazenil co-administration attenuated several remimazolam-associated findings; however, a specific mechanism was not established.
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2. In C5-heterozygous intercrosses, the proportion of C5-homozygous-null female offspring exceeds the expected Mendelian ratio.
PMID:日期:2026-09-17The complement system has functions beyond host defense, including roles in development and reproduction. However, the role of complement C5 in fertilization and early embryonic development remains unclear. Here, we investigated the reproductive phenotype of C5-deficient mice on a BALB/c background. C5 mice were fertile and showed no obvious reproductive abnormalities under standard laboratory housing conditions. However, offspring from C5 × C5 mating showed a significant deviation from the expected Mendelian distribution, with an increased proportion of female C5 offspring, whereas male offspring showed no comparable distortion. In vitro fertilization reproduced this skewed ratio which was detectable at the blastocyst stage, suggesting that the underlying mechanism operates during fertilization or preimplantation development. Parent-of-origin analysis further suggested a contribution of maternal C5. During preimplantation development, C5, C5a receptor 1 (C5ar1), and C5a receptor 2 (C5ar2) mRNA levels showed distinct dynamic expression profiles. These findings revealed an unexpected sex- and genotype-dependent reproductive phenotype associated with C5 deficiency and suggest that C5-dependent signaling may contribute to genotype-dependent selection during fertilization or preimplantation development. The dynamic expression of C5a receptors further supports a potential role for C5a signaling in early embryonic development and expands the biological role of complement beyond immune defense to include regulation of mammalian reproduction.
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3. IL-17RA deficiency improves diabetic wound healing and is associated with reduced oxidative stress, inflammation, and NF-κB/JMJD3-related signaling.
3. IL-17RA缺陷改善糖尿病创面愈合，并与氧化应激、炎症及NF-κB/JMJD3相关信号传导减少有关PMID:日期:2026-09-15Diabetic wound healing is delayed by a hostile wound microenvironment characterized by persistent oxidative stress, chronic inflammation, and dysfunction of key reparative cells, including keratinocytes, fibroblasts, endothelial cells, and immune cells. IL-17A/IL-17RA signaling is closely involved in diabetes-associated inflammation, but its role in diabetic wound repair remains incompletely defined. Male C57BL/6NCya-Il17ra knockout and age-matched wild-type (WT) mice were assigned to wild-type non-diabetic (WT-ND), Il17ra knockout non-diabetic (KO-ND), wild-type diabetic (WT-DM), and Il17ra knockout diabetic (KO-DM) groups. Diabetes was induced by streptozotocin, followed by dorsal full-thickness excisional wounding after confirmation of hyperglycemia. STZ-induced diabetic mice exhibited delayed wound closure, lower body weight, and persistently elevated fasting blood glucose. Compared with WT-DM mice, KO-DM mice showed significantly improved wound closure. Il17ra deficiency attenuated diabetes-associated oxidative stress, as indicated by higher SOD, catalase, and GSH levels and lower MDA levels, and reduced systemic and local IL-6, IL-1β, and TNF-α levels. At the molecular level, KO-DM wounds displayed reduced NF-κB p65 phosphorylation and JMJD3 expression, together with partial restoration of H3K27me3. In parallel, Il17ra deficiency suppressed diabetes-induced expression of Cxcl1, Cxcl5, Ccl20, Itga3, and Timp1 while partially restoring Mmp2 and Fgf2 expression. Histologically, KO-DM wounds showed smaller epithelial gaps, thicker granulation tissue, lower inflammatory scores, and greater collagen deposition than WT-DM wounds. Il17ra deficiency promotes diabetic wound healing and is associated with reduced oxidative stress and inflammation, accompanied by attenuation of NF-κB/JMJD3-related molecular and transcriptional abnormalities.
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4. Progressive islet remodeling during the prediabetic stage in female SDT rats.
4. 雌性SDT大鼠糖尿病前期阶段的进行性胰岛重塑PMID:日期:2026-09-12Prediabetes represents a critical stage in the progression to type 2 diabetes, during which early alterations in pancreatic islet structure and function occur. We investigated temporal histopathological changes associated with islet remodeling in female Spontaneously Diabetic Torii (SDT) rats, a non-obese type 2 diabetes model. Focusing on structural alterations, fibrosis, altered endocrine cell organization, and pancreatic stellate cell activation. Female SDT and Sprague-Dawley (SD) rats were examined between 8 and 40 weeks of age. Blood glucose and plasma insulin levels were measured cross-sectionally in separate groups of animals from 8 to 40 weeks, and oral glucose tolerance tests (OGTTs) were performed between 16 and 24 weeks of age. Pancreatic tissues were evaluated by histopathology, immunohistochemistry, and morphometric analyses. SDT rats exhibited progressive glucose intolerance accompanied by elevated plasma insulin levels during the prediabetic stage, suggesting altered glucose homeostasis. These abnormalities were accompanied by structural alterations of islets, including architectural disruption, enlargement, and intra-islet fibrosis beginning at 18-24 weeks. Representative immunostaining suggested altered organization of insulin- and glucagon-positive endocrine cells within remodeled islets. α-SMA- and desmin-positive stromal cells were observed within fibrotic regions of SDT islets. These findings demonstrate progressive islet remodeling during the prediabetic stage in female SDT rats, characterized by structural disruption, fibrosis, and the presence of α-SMA- and desmin-positive stromal cells within fibrotic islets. These alterations may contribute to early endocrine dysfunction by disrupting the islet microenvironment and cell-cell interactions.
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5. Remimazolam- and dexmedetomidine-based three-drug mixtures refine injectable anesthesia in mice.
5. 基于瑞马唑仑和右美托咪定的三药混合物优化小鼠注射麻醉PMID:日期:2026-09-11The medetomidine-midazolam-butorphanol mixture (MMB) is widely used for injectable anesthesia in mice but is associated with delayed induction, prolonged recovery, impaired oxygenation, and post-anesthetic hypothermia. We investigated whether substituting midazolam with remimazolam, alone or together with replacing medetomidine with dexmedetomidine, improved the anesthetic profile. Male C57BL/6JJcl mice (n=8/group) received intraperitoneal MMB, medetomidine-remimazolam-butorphanol (MRB), or dexmedetomidine-remimazolam-butorphanol (dMRB). Induction was assessed by times to immobilization and loss of the righting reflex (LORR), anesthetic depth by a study-specific 0-5 reflex-loss score, and recovery by time to return of the righting reflex (RORR). Oxygen saturation, heart rate, respiratory rate, and rectal temperature were monitored. Compared with MMB, MRB shortened times to immobilization, LORR, and RORR, whereas dMRB shortened LORR. The reflex-loss score showed no overall group effect or area under the curve (AUC) difference, although a significant interaction between group and time indicated different temporal profiles. No overall group main effects were detected for the physiological variables during anesthesia; however, measured SpO₂ was markedly low in all groups (pooled mean, 61.7 ± 6.6%). During recovery without external heating, rectal temperature differed among groups: the dMRB-MMB AUC comparison was significant, MRB-MMB was borderline, and MRB-dMRB was not significant. MRB improved induction and recovery timing, whereas dMRB improved induction and showed the strongest evidence of better recovery-phase thermoregulation; neither modification corrected the low measured SpO₂.
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6. Route-dependent immune-inflammatory and tissue remodeling responses to BCG injection in mice.
PMID:日期:2026-09-10Bacillus Calmette-Guérin (BCG) activates innate immune responses, but its tissue effects depend on the route of administration. We compared intra-airway (IA) and intravenous (IV) BCG administration in female C57BL/6N mice using a matched longitudinal design from immediately after administration through day 28. Outcomes included body and organ weights, gross pathology, histology, collagen and iron deposition, and pulmonary inflammatory-marker expression. IA-BCG reduced body-weight gain and produced marked pulmonary inflammation, collagen deposition, and increased staining for inflammatory and fibrosis-related markers. IV-BCG caused minimal pulmonary injury but produced hepatosplenomegaly, periportal hepatic collagen deposition, splenic hemorrhage, and splenic iron accumulation. These findings define distinct route-associated tissue phenotypes under matched experimental conditions. IA administration provides a model for pulmonary inflammation and remodeling, whereas IV administration provides a model for hepato-splenic responses. Bacterial burden, immune-cell composition, and causal signaling pathways were not assessed.
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7. Traditional Chinese herbal formula Huo Luo Xiao Ling Dan ameliorates rheumatoid arthritis by suppressing inflammation and oxidative stress via the AGE/RAGE/NF‑κB signaling pathway.
7. 传统中药复方活络效灵丹通过AGE/RAGE/NF-κB信号通路抑制炎症和氧化应激改善类风湿关节炎PMID:日期:2026-09-09Rheumatoid arthritis (RA) is a chronic autoimmune pathology that arises chiefly from the dysregulated activation of fibroblast-like synoviocytes. The traditional Chinese herbal formula Huo Luo Xiao Ling Dan (HLXL) has unclear mechanisms in RA treatment. This work combined network pharmacology with both cellular and animal-based experiments. Network analysis suggested the advanced glycation end products (AGE)/receptor for advanced glycation end products (RAGE) pathway as a crucial target for HLXL. In vitro experiments showed that HLXL (50, 100 μg/mL) dose‑dependently suppressed TNF‑α‑induced MH7A human fibroblast-like synoviocyte proliferation, migration, invasion, and NF‑κB activation. Additionally, HLXL reduced oxidative stress markers (ROS, MDA) and pro‑inflammatory cytokines (IL‑6, IL‑1β), while enhancing total superoxide dismutase (tSOD) activity. The RAGE agonist D‑Ribose counteracted these effects, confirming the involvement of AGE/RAGE signaling. In collagen‑induced arthritis (CIA) rats, HLXL (7.25, 14.5 g/kg) ameliorated joint swelling, arthritis index, synovial pathology, and cartilage erosion. It also decreased oxidative stress and inflammatory factors in serum and synovial tissues and suppressed AGE/RAGE/NF‑κB signaling in vivo. Collectively, HLXL exerts anti‑RA effects through inhibition of the AGE/RAGE/NF‑κB pathway.
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8. Spontaneous hepatocellular carcinoma in laboratory-reared degus (Octodon degus): histopathological and immunohistochemical characterization.
PMID:日期:2026-08-27The degu (Octodon degus), a highly intelligent rodent with unique communication abilities, has been used in various research fields. However, reports on spontaneous lesions in degus are limited. During routine examinations, we incidentally observed hepatic nodular lesions in laboratory-reared degus maintained at the University of Miyazaki. We aimed to investigate the prevalence and histopathological characteristics of hepatic nodular lesions in degus. The prevalence of these lesions increased with age, but no sex-related differences were observed. No gross abnormalities were noted in any organ other than the liver. Serum biochemistry revealed significantly higher aspartate aminotransferase levels in animals with hepatic nodules than in those without nodules. Histopathologically, the nodules were sharply demarcated from the normal hepatic parenchyma without fibrous encapsulation, and showed loss of lobular architecture and portal triads, along with markedly thickened hepatic cords. The nodular cells expressed arginase-1 and exhibited abundant clear cytoplasm, moderate anisocytosis, anisokaryosis, and glycogenated nuclei. Despite rare mitotic figures, the Ki67 labeling index of the neoplastic cells was significantly higher than that of normal hepatocytes. There was no evidence of epithelial mesenchymal transition in the lesions. Collectively, these hepatic nodules were diagnosed as spontaneously occurring, well-differentiated hepatocellular carcinomas. This is the first report to compile multiple cases of spontaneous hepatocellular carcinoma in degus. This study provides valuable background pathological information and supports the potential utility of degus as a laboratory animal model in hepatocellular neoplasia.
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9. CCDC85C expression in rat glomeruli and its role in kidney development.
PMID:日期:2026-08-25Coiled-coil domain containing 85c (CCDC85C), a protein located at cell junctions, has attracted attention for its role in regulating cellular differentiation and polarization. To clarify CCDC85C function, we previously established Ccdc85c knockout (KO) rats. Our previous studies reported that CCDC85C is expressed during the kidney development and that its expression gradually decreases as maturation. The finding implies that CCDC85C is involved in kidney development. However, CCDC85C localization and the detailed kidney histology of Ccdc85c KO animals remain unclear. In the present study, we examined the expression patterns of CCDC85C and the histological consequences of Ccdc85c KO rat kidneys. Immunofluorescence revealed that CCDC85C was expressed in glomeruli at 4, 25 and 50 weeks of age, and distal renal tubules at 4 weeks of age. CCDC85C consistently co-localized with a tight junction marker, zonula occludens-1 (ZO-1) in the podocytes at 4, 25, and 50 weeks of age. At 4 weeks of age, Ccdc85c KO rats showed a thin renal cortex, small and variable size of glomeruli, flattened podocytes and indistinct slit diaphragms. These immature histological features suggest developmental retardation (hypoplasia). In conclusion, CCDC85C is expressed in glomeruli with its presence persisting into late adulthood in rats. The specific localization of CCDC85C suggests its involvement in the tight junction compartment of podocyte foot processes, where it likely maintains the filtration barrier. We propose that CCDC85C is important for the proper development and structural maintenance of the rat kidney.
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10. Genome-wide identification of genetic modifiers of Pak1-dependent skin tumor susceptibility in mice.
PMID:日期:2026-08-21Pak1, a serine/threonine kinase, plays dual roles during the tumor progression and immune response. Unfortunately, the genetic modifiers underlying the resistance caused by Pak1 deficiency in CD11c-positive immune cells have been poorly defined so far. To adequately address this gap, we conducted a forward genetic screen using Cd11cCre-Pak1 F backcross mice (n=182). GRAS-Di-based genome-wide genotyping has identified 14,053 high-confidence markers, and we analyzed them by taking advantage of the principal component-adjusted generalized linear models (GLMs). Among the nine candidates of genome-wide significant Pak1 modifier loci (Pm1-Pm9) associated with tumor susceptibility, Pm1 on chromosome 5 showed the earliest and strongest association with the stages of papilloma and carcinoma. Intriguingly, epistasis analysis revealed that Pm3 on chromosome 4 attenuates the tumor-promoting effect of Pm1 in an allele-dependent manner, raising a possibility that the immune regulators modulate tumor susceptibility in Pak1-reduced immune compartment. Taken together, our present findings delineate a genetic framework implicated in Pm1/Pm3 axis during Pak1-reduced, skin carcinogenesis driven by immune response.