The increased motion of lumbar induces ligamentum flavum hypertrophy in a rat model

Abstract Background The purpose of this study was to establish a novel rat model for ligamentum flavum (LF) hypertrophy using increased motion of lumbar and to elucidate the etiology of (LFH). Methods A total number of 30 male rats were used. The increased motion of lumbar was induced by surgical resection of L5/6 posterior elements (n = 15). The other rats underwent a sham operation (n = 15). After 8 weeks, all rats were taken lateral plain X-rays. The LF from L5/6 in both groups were harvested to investigate histological, immunohistological, and real-time PCR analysis. Results According to radiological results, the disc height ratio, flexion ratio, and extension ratio were larger in the rats in the experimental group than that of in the sham group. The HE staining showed that the LF thickness in the experimental group significantly increased in comparison to the sham group. The Masson trichrome staining showed that the ratio of elastic fibers to collagen fibers in experimental group was lower than that in the sham group. The protein and gene expression of TGF-β1, TNF-α, IL-1β, and Col 1 were significantly higher in the experimental group than that in the sham group. Conclusion A relatively safe, simple, and rapid rat model of LFH using increased motion of lumbar was established. The increased motion of lumbar could lead to high expression of inflammatory and fibrotic factors in LF, causing the accumulation of collagen fibers and decreasing of elastic fibers.

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Lumbar Instability Induces Ligamentum Flavum Hypertrophy in a Rat Model

10.21203/rs.3.rs-140228/v1 ◽

2021 ◽

Author(s):

Baojian Wang ◽

Chunyu Gao ◽

Liguo Zhu ◽

Ping Zhang ◽

Wu Sun ◽

...

Keyword(s):

Rat Model ◽

Ligamentum Flavum ◽

Collagen Fibers ◽

Male Rats ◽

Elastic Fibers ◽

Control Group ◽

Sham Operation ◽

X Rays ◽

Lumbar Instability ◽

Experimental Group

Abstract Background: The purpose of this study was to establish a novel rat model for ligamentum flavum (LF) hypertrophy using lumbar instability and to elucidate the etiology of LF hypertrophy. Methods: A total number of 30 male rats were used. Lumbar instability was induced by surgical resection of L5/6 posterior elements (n=15). The other rats underwent a sham operation (n=15). After 8 weeks, all rats were taken lateral plain X-rays. The LF from L5/6 in both groups were harvested to investigate histological, immunohistological, and real-time PCR analysis. Results: According to radiological results, the disc height ratio and extension ratio were larger in the rats in the experimental group than that of in the control group. The HE staining showed that the LF thickness in the experimental group significantly increased in comparison to the control group. The Masson trichrome staining showed that the ratio of elastic fibers to collagen fibers in experimental group was lower than that in the control group. The protein and gene expression of TGF-β1, TNF-α, IL-1β, and Col 1 were significantly higher in the experimental group than that in the control group. Conclusion: It is the first time that lumbar instability directly induced LF hypertrophy in a reproducible rat model. Lumbar instability could lead to high expression of inflammatory and fibrotic factors in LF, causing the accumulation of collagen fibers and decreasing of elastic fibers.

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Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01120.2008 ◽

2009 ◽

Vol 296 (4) ◽

pp. H1117-H1124 ◽

Cited By ~ 16

Author(s):

Yoshiaki Takewa ◽

Elie R. Chemaly ◽

Miyako Takaki ◽

Li Fan Liang ◽

Hongwei Jin ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Remodeling ◽

Sham Group ◽

Group Versus ◽

Volume Overload ◽

Left Ventricular ◽

Mechanical Work ◽

Energy Utilization ◽

Male Rats ◽

Sham Operation

Eccentric cardiac remodeling seen in dilated cardiomyopathy or regurgitant valvular disease is a well-known process of heart failure progression, but its mechanoenergetic profile has not been yet established. We made a volume overload (VO) heart failure model in rats and for the first time investigated left ventricular (LV) mechanical work and energetics in cross-circulated whole heart preparations. Laparotomy was performed in 14 Wistar male rats, and abdominal aortic-inferior vena caval shunt was created in seven rats (VO group). Another seven rats underwent a sham operation without functional shunt (Sham group). LV dimensions changes were followed with weekly transthoracic echocardiography. Three months after surgery, we measured LV pressure and volume and myocardial O2 consumption in isolated heart cross circulation. LV internal dimensions in both systolic and diastolic phases were significantly increased in the VO group versus the Sham group ( P < 0.05). LV pressure was markedly decreased in the VO group versus in the Sham group ( P < 0.05). LV end-systolic pressure-volume relation shifted downward, and myocardial O2 consumption related to Ca2+ handling significantly decreased. The contractile response to Ca2+ infusion was attenuated. Nevertheless, the increase in Ca2+ handling-related O2 consumption per unit change in LV contractility in the VO group was significantly higher than that in the Sham group ( P < 0.05). The levels of sarco(endo)plasmic reticulum Ca2+-ATPase 2a protein were reduced in the VO group ( P < 0.01). In conclusion, VO failing rat hearts had a character of marked contractile dysfunction accompanied with less efficient energy utilization in the Ca2+ handling processes. These results suggest that restoring Ca2+ handling in excitation-contraction coupling would improve the contractility of the myocardium after eccentric cardiac remodeling.

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Prevention of Progression of Aortic Aneurysm by Peptide Vaccine Against Ang II (Angiotensin II) in a Rat Model

Hypertension ◽

10.1161/hypertensionaha.119.14442 ◽

2020 ◽

Vol 76 (6) ◽

pp. 1879-1888

Author(s):

Tomohiro Kurashiki ◽

Takashi Miyake ◽

Hironori Nakagami ◽

Motonobu Nishimura ◽

Ryuichi Morishita

Keyword(s):

Angiotensin Ii ◽

Aortic Aneurysm ◽

Rat Model ◽

Peptide Vaccine ◽

Male Rats ◽

Matrix Metalloproteinase 2 ◽

Elastic Fibers ◽

Aortic Dilatation ◽

Ang Ii ◽

Aneurysm Wall

There is no proven medical therapy to inhibit the progression of abdominal aortic aneurysm (AAA) in the clinical setting. To develop a novel therapeutic approach for the treatment of AAA, we focused on vaccination targeting Ang II (angiotensin II) and assessed the effect of an Ang II peptide vaccine on the progression of AAA using a rat model. Ang II peptide was conjugated with KLH (keyhole limpet hemocyanin) carrier protein to induce a sufficient immune response. Male rats were subcutaneously immunized with Ang II–KLH with an adjuvant on days 0, 14, and 28. Aortic dilatation was induced by intraluminal incubation with elastase on day 35. Treatment with Ang II vaccine successfully induced the production of a high titer of anti-Ang II antibodies. Immunization with Ang II vaccine resulted in a significant reduction in expansion of the aortic diameter compared with control rats, without a blood pressure–lowering effect. Four weeks after operation, the increase in Ang II in the aneurysm wall was significantly inhibited by treatment with Ang II vaccine. Inhibition of Ang II action led to suppression of the inflammatory response in the AAA wall through attenuation of the NFκB (nuclear factor kappa B) and c-jun N-terminal kinase signaling cascades. Treatment with Ang II vaccine inhibited accumulation of macrophages in the AAA wall. In addition, expression of TNF-α (tumor necrosis factor alpha) and activation of MMP (matrix metalloproteinase)-2 and MMP-9 were also inhibited by treatment with Ang II vaccine, resulting in protection against the destruction of elastic fibers. This vaccine therapy could become a potent therapeutic option to treat patients with AAA.

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Bsep expression in hilar cholangiocarcinoma of rat model

Scientific Reports ◽

10.1038/s41598-021-82636-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Meng-yu Zhang ◽

Jie-ping Wang ◽

Kai He ◽

Xian-ming Xia

Keyword(s):

Bile Duct ◽

Rat Model ◽

Hilar Cholangiocarcinoma ◽

Pathological Examination ◽

Control Group ◽

Sham Operation ◽

Sham Operation Group ◽

Hilar Bile Duct ◽

Operation Group ◽

Experimental Group

AbstractDevelop a rat model of hilar cholangiocarcinoma for detecting bile salt export pump (Bsep) expression in hilar cholangiocarcinoma tissues, in order to provide a new therapeutic target for the gene therapy of hilar cholangiocarcinoma. Sixty male Wistar rats (body weight, 190 ± 8 g) were randomly divided into three groups (the experimental group, the control group and the sham operation group, n = 20 each) as follows: The three groups were fed a standard diet, the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe, the control group was injected by normal saline, the sham operation group did not inject anything. Every day assess the rats’ mental state, diet, and motion by using Basso–Beattie–Bresnahan and combined behavioral score. At 4 weeks, one rat of the experimental group was sacrificed after it was administered anesthesia, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of Bsep in hilar bile duct tissues of each group. From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with control group and sham operation group. After 6 weeks, we detected hilar cholangiocarcinoma in the hilar bile duct tissues of 18 rats (90%) in the experimental group. In the experimental group with hilar cholangiocarcinoma, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those in the control group and sham operation group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The Bsep/Gapdh mRNA ratio in hilar cholangiocarcinoma, control group and sham operation group differed markedly. Light microscopy revealed a granular pattern of Bsep protein expression which reacted with the anti-Bsep antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with > 10% positive cells were designated positive, Sections with < 10% positive cells were designated negative. Each group included 4800 cells. In the experimental group, 1200 cells (25%) were positive, in the control group, 3648 cells (76%) were positive and in the sham operation group 3598 cells (75%) were positive, and this difference was statistically significant. Bsep expression significantly decreased in hilar cholangiocarcinoma of rats than those in control group and sham operation group, suggesting that drugs targeting Bsep are a new strategy for hilar cholangiocarcinoma.

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Protection of Liver as a Remote Organ after Renal Ischemia-Reperfusion Injury by Renal Ischemic Postconditioning

International Journal of Nephrology ◽

10.1155/2014/120391 ◽

2014 ◽

Vol 2014 ◽

pp. 1-4 ◽

Cited By ~ 8

Author(s):

Behjat Seifi ◽

Mehri Kadkhodaee ◽

Atefeh Najafi ◽

Atefeh Mahmoudi

Keyword(s):

Oxidative Stress ◽

Liver Damage ◽

Sham Group ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Ischemic Postconditioning ◽

Male Rats ◽

Sham Operation ◽

Sod Activity ◽

Remote Organ

This study was designed to investigate the protective effects of local renal ischemic postconditioning (POC) on liver damage after renal ischemia-reperfusion (IR) injury. Male rats were divided into three groups (n=8). They underwent a right nephrectomy before induction of 45 minutes of left kidney ischemia or sham operation. POC was performed by four cycles of 10 seconds of ischemia and 10 seconds of reperfusion just at the beginning of 24 hours of reperfusion. Then blood and liver samples were collected to measure serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and liver oxidative stress parameters including superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Renal IR caused a significant increase in liver functional indices as demonstrated by increased serum AST and ALT compared to sham group. These parameters reduced significantly in POC group compared to IR group. Liver MDA levels increased and SOD activity decreased in IR group compared to sham group. Induction of POC reduced the elevated liver MDA levels and increased the reduced liver SOD activity. These results revealed that renal IR injury causes liver damage as a remote organ and POC protects liver from renal IR injury by a modification in the hepatic oxidative stress status.

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Bioinformatics Study of Osteoclastogenesis Inhibitory Factor and Receptor Activator of NF-κB Ligand Expression in Ovariectomized Osteoporosis Rat Model Using Probiotics Preparation

Journal of Medical Imaging and Health Informatics ◽

10.1166/jmihi.2019.2786 ◽

2019 ◽

Vol 9 (8) ◽

pp. 1553-1562

Author(s):

Jingteng He ◽

Qing Xu ◽

Yanchao Zhang ◽

Xu Chen ◽

Xiaoyu Jia ◽

...

Keyword(s):

Medical Imaging ◽

Protein Expression ◽

Rat Model ◽

Sham Group ◽

Intervention Group ◽

Female Rats ◽

Control Group ◽

Intragastric Administration ◽

Sham Operation ◽

Ovx Rats

Objective: To study the expression of OPG and RANKL in the ovariectomized osteoporosis SD rat model by probiotics preparation, and to observe the mechanism of probiotics regulating bone metabolism by medical imaging, and finally improve and improve the bone mass level of the elderly. Methods: Forty five 12 weeks old SD female rats were randomly were evenly divided into control group (Sham operation, Sham), ovariotomy group (Ovariectomy, the OVX), ovarian resection and probiotic preparations intervention group (OVX + Probiotics), each group of 15, in addition to the Sham group ovaries removed around the same size of adipose tissue, the OVX + Probiotics group and the OVX rats were performed bilateral ovaries removed. Eight weeks after the surgery, each group randomly, 2 rats dual-energy X-ray absorptiometry measurement, determine after the success of the building, the OVX + Probiotics group feed gavage quad living bacterium equivalent dose concentration solution, Sham group and the OVX group was given distilled water filling and feed volume. After 4 weeks of continuous administration, all rats were sacrificed. Subsequently, Tb. N, Tb. Th, Tb. Sp and BV/TV were measured by micro-CT of medical imaging technique. The levels of serum BGP, ALP and Ca were measured by automatic biochemical analyzer. Real-time quantitative PCR and the expression levels of OPG, β-actin and RANKL genes and proteins were detected by Western blot. Results: Compared with the Sham group, compared with the, the OVX + Probiotics group and the OVX rats femur lower Tb. N, Tb. Th, BV/TV value decreased significantly, Tb. Sp increased significantly, serum BGP and ALP, Ca levels were significantly lower (P < 0.05), the OVX + Probiotics group compared with OVX group, the rat femur lower Tb. N, Tb. Th, BV/TV value, Tb. Sp, reducing RANKL protein expression and serum BGP and ALP, Ca levels, OPG protein expression were higher. The difference was statistically significant (P < 0 05), after 4 weeks intragastric administration. Conclusion: The probiotic preparation (Bifidobacterium quadruple live bacteria) has an effect on the OPG/RANKL/RANK axis system, which plays an anti-OP role, and provides a new research direction for the prevention and treatment of postmenopausal osteoporosis.

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Abstract 329: N-acetylcyteine Alleviate Inflammasome-Induced Myocardial Pyroptosis After Successful Resuscitation in a Rat Model of Cardiac Arrest

Circulation ◽

10.1161/circ.138.suppl_2.329 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Fenglian He

Keyword(s):

Cardiac Arrest ◽

Western Blotting ◽

Rat Model ◽

Sham Group ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Male Rats ◽

Control Group ◽

Successful Resuscitation ◽

Caspase 1

Introduction: Previous studies have demonstrated that pyroptosis is involved in myocardial ischemia/reperfusion injury (MIRI). In addition, N-acetylcyteine (NAC) can attenuate inflammasome-induced pyroptosis during regional MIRI. In the present study, we investigated whether pyroptosis participate in global MIRI after successful resuscitation, and if it does, whether NAC can reduce inflammasome-induced pyroptosis in a rat model of cardiac arrest and resuscitation. Hypothesis: N-acetylcyteine reduces inflammasome-induced myocardial pyroptosis after successful resuscitation in a rat model of cardiac arrest. Methods: Fifteen male rats weighing 450g-550g were randomized into three groups: sham group, control group and NAC group (150 mg/kg). Ventricular fibrillation (VF) was electrically induced and untreated for 8 min. After VF, CPR was initiated for 8 mins and then defibrillation was attempted. Animals in sham group only were underwent the same operation but without inducing CA. The expressions of Nod-like receptor protein3 (NLRP3), adaptor apoptosis-associated speck-like protein (ASC), caspase-1 and gasdermin D (GSDMD) proteins were detected by western blotting at 6h following successful resuscitation. Results: All animals were resuscitated. Significantly higher levels expressions of GSDMD, NLRP3, ASC and caspase-1 were observed in control group and NAC group when compared with sham group. However, the expressions in GSDMD, NLRP3, ASC and caspase-1 were downregulated in NAC group in comparison with the control group. (Figure) Conclusion: N-acetylcyteine attenuate inflammasome-induced myocardial pyroptosis after successful resuscitation in a rat model of cardiac arrest. Figure Expressions of GSDMD, NLRP3, ASC and caspase-1 proteins, and effect of NAC on cardiac pyroptosis after successful resuscitation in a rat model of CA. (A) Representative western blotting images of GSDMD, NLRP3, ASC and caspase1 proteins in the hearts at 6h after successfully resuscitated (B) Quantitative protein analysis of GSDMD, NLRP3, ASC and caspase1 expression in three groups. The columns represent means ± SEM of three independent experiments. * p < .05

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Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

International Journal of Molecular Sciences ◽

10.3390/ijms22073762 ◽

2021 ◽

Vol 22 (7) ◽

pp. 3762

Author(s):

Sarah M. Kedziora ◽

Kristin Kräker ◽

Lajos Markó ◽

Julia Binder ◽

Meryam Sugulle ◽

...

Keyword(s):

Rat Model ◽

Renal Damage ◽

Kidney Injury ◽

Tissue Growth ◽

Female Rats ◽

Male Rats ◽

Renal Diseases ◽

Transgenic Rat ◽

Increased Risk ◽

Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

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Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

Experimental Biology and Medicine ◽

10.1177/1535370221995207 ◽

2021 ◽

pp. 153537022199520

Author(s):

Nanees F El-Malkey ◽

Amira E Alsemeh ◽

Wesam MR Ashour ◽

Nancy H Hassan ◽

Husam M Edrees

Keyword(s):

Oxidative Stress ◽

Rat Model ◽

Intestinal Ischemia ◽

Ischemia Reperfusion ◽

Protective Role ◽

Beclin 1 ◽

Male Rats ◽

Fetuin A ◽

Intestinal Ischemia Reperfusion ◽

And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

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Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/507091 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 4

Author(s):

Jin-hui Li ◽

Jing Lu ◽

Hong Zhang

Keyword(s):

Cerebral Ischemia ◽

Rat Model ◽

Neurological Deficit ◽

Neuronal Maturation ◽

Vascular Density ◽

Sham Operation ◽

Therapeutic Effects ◽

Neuroprotective Effects ◽

Neuronal Marker ◽

Cerebral Ischemic

Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry.Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P<0.001).18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P<0.01) and Scu-25 group (P<0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation.Conclusion.18F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.

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