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The Sugen 5416/hypoxia (Su/Hx) rat model of pulmonary arterial hypertension (PAH) demonstrates most of the distinguishing features of PAH in humans, including increased wall thickness and obstruction of the small pulmonary arteries along with plexiform lesion formation. Recently, significant advancement has been made describing the epidemiology, genomics, biochemistry, physiology, and pharmacology in Su/Hx challenge in rats. For example, there are differences in the overall reactivity to Su/Hx challenge in different rat strains and only female rats respond to estrogen treatments. These conditions are also encountered in human subjects with PAH. Also, there is a good translation in both the biochemical and metabolic pathways in the pulmonary vasculature and right heart between Su/Hx rats and humans, particularly during the transition from the adaptive to the nonadaptive phase of right heart failure. Noninvasive techniques such as echocardiography and magnetic resonance imaging have recently been used to evaluate the progression of the pulmonary vascular and cardiac hemodynamics, which are important parameters to monitor the efficacy of drug treatment over time. From a pharmacological perspective, most of the compounds approved clinically for the treatment of PAH are efficacious in Su/Hx rats. Several compounds that show efficacy in Su/Hx rats have advanced into phase II/phase III studies in humans with positive results. Results from these drug trials, if successful, will provide additional treatment options for patients with PAH and will also further validate the excellent translation that currently exists between Su/Hx rats and the human PAH condition.

The aim of this research was to investigate the effect of amygdalin on hepatic fibrosis in rats. Amygdalin was purified and identified from the seeds of . Sprague Dawley rats in the control and model groups were administered water. Sprague Dawley rats were divided into the low-, middle-, and high-dose amygdalin groups that received 20, 40, and 80 mg kg amygdalin, respectively. whereas the silymarin group was treated with 50 mg kg silymarin. The control and model groups were administered water. Liver tissue analysis revealed significantly lower activities of ALT, AST, ALP, SOD, and MDA in the drug-treated groups compared to the model group. Serum analysis revealed significantly lower HYC and C-IV in the middle-dose amygdalin-treated group compared to the model group. The histopathological changes were less severe in the drug-treated groups as observed by the formation of pseudolobuli and decreased collagen fiber deposition. Hepatic fibrosis-related genes were expressed at significantly lower levels in the amygdalin-treated groups than in the model group. Amygdalin from represents a therapeutic candidate for hepatic fibrosis prevention and treatment.

Background Zucker diabetic fatty (ZDF) rats exhibit significant phenotypic variability despite genetic uniformity, yet a comprehensive characterization of these divergent phenotypes remains limited. Methods Male ZDF (fa/fa) rats (4 months, n = 22) and ZDF (fa/+) lean controls (n = 10) were maintained on standard chow for 6 months. Based on metabolic trajectory, ZDF (fa/fa) rats were stratified into three phenotypes: obese normoglycemic (O, n = 8), diabetic with cachexia (D, n = 8), and diabetic without cachexia (D‐C, n = 6). Comprehensive assessments included body weight, glycemic control, hepatic function, oxidative stress markers, and inflammatory cytokines. Results Principal coordinate analysis confirmed significant metabolic separation between phenotypes (p < 0.01). Diabetic cachectic (D) rats exhibited severe hyperglycemia (>25 mmol/L), insulin depletion, elevated hepatic enzymes (alanine aminotransferase [ALT] increased 2.5‐fold, p < 0.01), elevated interleukin‐6, and delayed pain response. Diabetic rats without cachexia (D‐C) exhibited intermediate hyperglycemia (≈13 mmol/L, p < 0.001 vs. control) with preserved insulin levels, and elevated fibroblast growth factor 21 (FGF21) and soluble receptor for advanced glycation end products (sRAGE). Obese normoglycemic (O) rats maintained normoglycemia with hyperinsulinemia and elevated triglycerides. Conclusion Under identical genetic and environmental conditions, ZDF (fa/fa) rats develop distinct metabolic phenotypes encompassing euglycemic obesity, pre‐cachectic diabetes, and advanced cachectic diabetes. Phenotypic stratification is essential for accurate interpretation of ZDF experimental data and underscores the importance of characterizing individual metabolic trajectories when diabetic complications and therapeutic interventions are assessed in this model. Genetically uniform Zucker Diabetic Fatty (ZDF) rats spontaneously develop four distinct metabolic phenotypes despite identical housing and diet conditions. Each phenotype exhibits unique biomarker signatures encompassing glucose homeostasis, insulin secretion, polyol pathway activation, oxidative stress, inflammatory cytokines, and neurotrophic factors. This intrinsic heterogeneity has critical implications for experimental design, animal stratification, and translational interpretation in diabetes research. Visual layout: The graphical presents a longitudinal developmental schematic showing phenotypic divergence in ZDF rats across a 10‐month timeline (months 5–10). Starting from a uniform baseline population (left), genetically identical fa/fa rats diverge into three metabolically distinct phenotypes, while fa/+ controls maintain stable characteristics. Four color‐coded phenotypes: Red panel (Diabetic‐Cachectic, D): Severe diabetes with weight loss, hyperglycemia, hyperinsulinemia, elevated polyol pathway activity (↑sorbitol), pro‐inflammatory profile (↑IL‐6, ↓IL‐10), tissue oxidative stress (altered GSH distribution), and elevated neurotrophic factors (↑BDNF, ↑β‐NGF). Orange panel (Diabetic‐Non‐Cachectic, D‐C): Moderate diabetes with preserved body weight, hyperglycemia with compensatory hyperinsulinemia, intermediate metabolic stress markers, maintained inflammatory‐oxidative balance. Yellow panel (Obese‐Metabolically Protected, O): Obesity without overt diabetes, improved glucose tolerance compared to diabetic groups, lowest inflammatory activation, preserved antioxidant capacity, minimal neurological impairment. Blue panel (Lean Control, C): fa/+ heterozygotes with normal metabolic profile, balanced inflammatory‐antioxidant status, baseline reference phenotype.

To observe the changes of Nogo/NgR and Rho/ROCK signaling pathway-related gene and protein expression in rats with spinal cord injury (SCI) treated with electroacupuncture (EA) and to further investigate the possible mechanism of EA for treating SCI. Allen's method was used to create the SCI rat model. Sixty-four model rats were further subdivided into four subgroups, namely, the SCI model group (SCI), EA treatment group (EA), blocking agent Y27632 treatment group (Y27632) and EA+blocking agent Y27632 treatment group (EA+Y), according to the treatment received. The rats were subjected to EA and/or blocking agent Y27632 treatment. After 14 days, injured spinal cord tissue was extracted for analysis. The mRNA and protein expression levels were determined by real-time fluorescence quantitative PCR and Western blotting, respectively. Cell apoptosis changes in the spinal cord were evaluated by in situ hybridization. Hindlimb motor function in the rats was evaluated by Basso-Beattie-Bresnahan assessment methods. Except for RhoA protein expression, compared with the SCI model group, EA, blocking agent Y27632 and EA+blocking agent Y27632 treatment groups had significantly reduced mRNA and protein expression of Nogo-A, NgR, LINGO-1, RhoA and ROCK II in spinal cord tissues, increased mRNA and protein expression of MLCP, decreased p-MYPT1 protein expression and p-MYPT1/MYPT1 ratio, and caspase3 expression, and improved lower limb movement function after treatment for 14 days (P<0.01 or <0.05). The combination of EA and the blocking agent Y27632 was superior to EA or blocking agent Y27632 treatment alone (P < 0.01 or <0.05). EA may have an obvious inhibitory effect on the Nogo/NgR and Rho/ROCK signaling pathway after SCI, thereby reducing the inhibition of axonal growth, which may be a key mechanism of EA treatment for SCI.

Impulsivity is an understudied area of post‐traumatic stress disorder, a debilitating disorder specifically associated with stress. We examined reward‐related impulsive behavior, anxiety‐like behavior, locomotor activity and social behavior in the absence and presence of protracted pharmacological positive modulation of α5‐ and α6‐GABAA receptors (GL‐II‐73 and DK‐I‐56‐1, respectively) in male Sprague–Dawley rats exposed to a combination of maternal deprivation (MD) and single prolonged stress (SPS). While locomotor and anxiety‐like behavior were not affected in the SPS and MD+SPS groups, the double‐hit group treated with DK‐I‐56‐1 exhibited a higher locomotor distance compared with MD+SPS and a higher percentage of open‐arm time in the elevated plus maze compared with the control group. In the variable delay‐to‐signal task of impulsivity, the total number of successful trials and premature responses (PR) in the first stage of the test day were reduced in all groups exposed to stress compared with the controls. Based on PR rates in the first and second set of trials, motor impulsivity was apparently suppressed in all stressed groups, while delay intolerance was suppressed only in the MD+SPS+GL‐II‐73 group, respectively. In the three‐chamber test, social interaction was completely normal, while social recognition was preserved in the MD+SPS+GL‐II‐73 group. In the resident‐intruder test, social play was reduced only in the SPS group. The evaluation of impulsive behavior in the used complex task was hindered by the lack of motivation of stressed rats, which in the case of omission percentage was ameliorated by positive modulation of α5 and α6 GABAA receptors. A double‐hit stress model in Sprague–Dawley rats induces alterations in motivation, motor impulsivity, and social recognition that are partially ameliorated by α5‐ and α6‐GABAA receptor modulation, suggesting domain‐specific effects of this modulation on the stress‐induced phenotype.

Forty-three rats were randomly assigned to the following four groups: non-ischemic group (Control Group), 1 cm-long ischemic group (Group 1), 2 cm-long ischemic group (Group 2), and 3 cm-long ischemic group (Group 3). The rates of AL were 0% (0/10) in the Control Group, 22.2% (2/9) in Group 1, 25% (2/8) in Group 2, and 50% (4/8) in Group 3. The bursting pressure of the Control Group was significantly higher than that of the other groups (p < 0.01). Regarding the pathological findings, the granulation thickness and the number of blood vessels at the anastomosed site were significantly higher in the Control Group than in Group 3 (p < 0.05). Receiver operating characteristics analysis revealed that Slope was the most significant predictor of AL, with an area under the curve of 0.861. When the cutoff value of Slope was 0.4, the sensitivity and specificity for the prediction of AL were 75% and 81.4%, respectively. Quantitative analysis of ICG fluorescence angiography could predict AL in a rat model.

The use of autologous nerve grafts remains the gold standard for treating nerve defects, but current nerve repair techniques are limited by donor tissue availability and morbidity associated with tissue loss. Recently, the use of conduits in nerve injury repair, made possible by tissue engineering, has shown therapeutic potential. We manufactured a biodegradable, collagen-based nerve conduit containing decellularized sciatic nerve matrix and compared this with a silicone conduit for peripheral nerve regeneration using a rat model. The collagen-based conduit contains nerve growth factor, brain-derived neurotrophic factor, and laminin, as demonstrated by enzyme-linked immunosorbent assay. Scanning electron microscopy images showed that the collagen-based conduit had an outer wall to prevent scar tissue infiltration and a porous inner structure to allow axonal growth. Rats that were implanted with the collagen-based conduit to bridge a sciatic nerve defect experienced significantly improved motor and sensory nerve functions and greatly enhanced nerve regeneration compared with rats in the sham control group and the silicone conduit group. Our results suggest that the biodegradable collagen-based nerve conduit is more effective for peripheral nerve regeneration than the silicone conduit.

Recently, exploitation of cerebrospinal fluid (CSF) circulation has become increasingly recognized as a feasible strategy to solve the challenges involved in drug delivery for treating brain tumors. Boron neutron capture therapy (BNCT) also faces challenges associated with the development of an efficient delivery system for boron, especially to brain tumors. Our laboratory has been developing a system for boron delivery to brain cells using CSF, which we call the “boron CSF administration method”. In our previous study, we found that boron was efficiently delivered to the brain cells of normal rats in the form of small amounts of L-p-boronophenylalanine (BPA) using the CSF administration method. In the study described here, we carried out experiments with brain tumor model rats to demonstrate the usefulness of the CSF administration method for BNCT. We first investigated the boron concentration of the brain cells every 60 min after BPA administration into the lateral ventricle of normal rats. Second, we measured and compared the boron concentration in the melanoma model rats after administering boron via either the CSF administration method or the intravenous (IV) administration method, with estimation of the T/N ratio. Our results revealed that boron injected by the CSF administration method was excreted quickly from normal cells, resulting in a high T/N ratio compared to that of IV administration. In addition, the CSF administration method resulted in high boron accumulation in tumor cells. In conclusion, we found that using our developed CSF administration method results in more selective delivery of boron to the brain tumor compared with the IV administration method.

Background: Scald burns are common thermal injuries in clinical settings, yet existing animal models lack standardization in burn size, exposure time, and severity control. Traditional burn induction methods, such as manual immersion or heated metal contact, suffer from high variability, limited reproducibility, and are operator-dependent, reducing their translational relevance. This study presents RAPID-3D (rat printed induction device—3D), a novel 3D-printed system designed to induce uniform and reproducible scald burns in a rat model, ensuring precise exposure control and minimal variability. Methods: RAPID-3D features four burn exposure windows (10 × 20 mm each, 10 mm spacing), allowing for controlled boiling water (100 °C, 8 s) exposure while immobilizing the anesthetized rat’s dorsum. N = 10 female Wistar rats were subjected to eight controlled burns per animal. Internal unburned control areas were used in each rat for intra-animal comparison. Burn evolution was assessed using digital planimetry, histological evaluation, and real-time microvascular perfusion analysis via laser Doppler line scanning (LDLS) at 1 h, which was repeated on day 4, 9 and 21 post-burn. Results: RAPID-3D generated highly consistent burn sizes (198 ± 3.54 mm2) across all rats, with low inter-animal variability. Histological analysis confirmed full-thickness epidermal necrosis and deep partial-thickness dermal damage (600–900 µm depth). Microvascular Trends: Perfusion dropped immediately post-burn, remained low at day 4, and gradually increased from day 9 onward, suggesting progressive neovascularization and vascular remodeling. RAPID-3D provides a standardized, reproducible, and clinically relevant scald burn model, eliminates operator-induced variability, enhances experimental consistency, and offers strong translational relevance for burn treatment development and wound healing research.

We aimed to establish a novel rat model of seminal vesiculitis that would provide an effective approach to investigate the pathogenesis of this disease in the future. Eight male rats received the same operation, during which the root of one of the two seminal vesicles was partly ligatured with sutures and the other vesicle was left intact. The samples of seminal vesicles were harvested on the 8th day following the operation. Hematoxylin and eosin and Masson's trichrome stains were used to observe the histopathology and the presence of fibrous tissue in seminal vesicles, respectively. Immunoblotting and immunohistochemistry were applied to determine the tumor necrosis factor-alpha and cyclooxygenase-2 levels in seminal vesicle tissues. Real-time fluorescence quantitative polymerase chain reaction was performed to measure the gene expression levels of proinflammatory cytokines. H2O2levelsin the seminal plasma from the seminal vesicle were also measured. Hematoxylin and eosin staining suggested that there was inflammatory cell infiltration into the seminal vesicles treated by partial root ligation. The tumor necrosis factor-alpha and cyclooxygenase-2 proteins were significantly upregulated in the treated seminal vesicles. The tumor necrosis factor-alpha, cyclooxygenase, interleukin 6, and inducible nitric oxide synthase mRNA expression levels were also upregulated in the treated seminal vesicles. The H2O2 levels in the seminal plasma from seminal vesicles with partial root ligation were significantly elevated compared with those from vesicle left intact. In conclusion, partially ligating the root of the seminal vesicle via sutures in rats is an effective method to establish a seminal vesiculitis rat model.