Effect of Kang Fu Yan capsule on phenol mucilage-induced intrauterine adhesion injury in female rats

Purpose: To investigate the effect of Kang fu yan capsule (KFYC) on phenol mucilage-induced intrauterine adhesion (IUA) in a rat model, and the underlying mechanisms. Methods: An IUA model was established by injecting 0.06 mL of 25 % phenol mucilage into the uterus of female Sprague-Dawley rats. The IUA model rats (n=59) were randomly divided into 5 groups: IUA group, fuke qianjin tablet group (FKQJT, 0.22 mg/kg), and 3 KFYC groups given different doses of the drug i.e. 0.13, 0.39and 1.17 mg/kg. A group of 10 healthy female rats served as control. After 19 days treatment, blood samples were collected for determination of IL-2 and IL-10 by ELISA, while uterine tissues were subjected to histological examination using hematoxylin and eosin staining (H&E) and Masson staining. Expressions of Notch1, recombination signal binding protein-JK (RBP-JK), a disintegrin and metalloprotease (ADAM)-12, ADAM-15, matrix metalloprotein-9 (MMP-9), and inhibitor of NF-κB (IĸB) in uterine tissues were determined using RT-qPCR and western blot analysis. Results: Compared to IUA group, histological results showed reduced inflammatory cell infiltration in rat uterine tissue of KFYC group. Moreover, KFYC significantly reversed uterine fibrosis (p < 0.05). Serum concentrations of IL-2 significantly decreased in KFYC groups (p < 0.05 or p < 0.01), and there was significant increases the serum concentrations of IL-10 in KFYC groups (p < 0.05 or < 0.01), when compared to IUA group. The mRNA and protein expressions of Notch1, RBP-JK, ADAM-12, ADAM-15, MMP-9 were also significantly down-regulated (p < 0.05), while protein expression of IĸB was upregulated in KFYC group, when compared to IUA group. Conclusion: KFYC exerts an anti-IUA effect via amelioration of uterine inflammation and fibrosis, probably via a mechanism involving regulation of Notch1/ADAM pathway.

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Aerobic Exercise Prevents Depression via Alleviating Hippocampus Injury in Chronic Stressed Depression Rats

Brain Sciences ◽

10.3390/brainsci11010009 ◽

2020 ◽

Vol 11 (1) ◽

pp. 9

Author(s):

Jie Kang ◽

Di Wang ◽

Yongchang Duan ◽

Lin Zhai ◽

Lin Shi ◽

...

Keyword(s):

Aerobic Exercise ◽

Mild Stress ◽

Glutamatergic System ◽

Sprague Dawley ◽

Bdnf Expression ◽

Sprague Dawley Rats ◽

Immobility Time ◽

Neurotoxic Effects ◽

Swimming Test ◽

Underlying Mechanisms

(1) Background: Depression is one of the overwhelming public health problems. Alleviating hippocampus injury may prevent depression development. Herein, we established the chronic unpredictable mild stress (CUMS) model and aimed to investigate whether aerobic exercise (AE) could alleviate CUMS induced depression-like behaviors and hippocampus injury. (2) Methods: Forty-eight healthy male Sprague-Dawley rats (200 ± 20 g) were randomly divided into 4 groups (control, CUMS, CUMS + 7 days AE, CUMS + 14 days AE). Rats with AE treatments were subjected to 45 min treadmill per day. (3) Results: AE intervention significantly improved CUMS-induced depressive behaviors, e.g., running square numbers and immobility time assessed by the open field and forced swimming test, suppressed hippocampal neuron apoptosis, reduced levels of phosphorylation of NMDA receptor and homocysteine in hippocampus, as well as serum glucocorticoids, compared to the CUMS rats. In contrast, AE upregulated phosphorylation of AMPAR receptor and brain-derived neurotrophic factor (BDNF) hippocampus in CUMS depression rats. The 14 day-AE treatment exhibited better performance than 7 day-AE on the improvement of the hippocampal function. (4) Conclusion: AE might be an efficient strategy for prevention of CUMS-induced depression via ameliorating hippocampus functions. Underlying mechanisms may be related with glutamatergic system, the neurotoxic effects of homocysteine, and/or influences in glucocorticoids-BDNF expression interaction.

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Serum concentrations of fully and undercarboxylated osteocalcin do not vary between estrous cycle stages in Sprague–Dawley rats

Endocrine ◽

10.1007/s12020-013-0008-x ◽

2013 ◽

Vol 44 (3) ◽

pp. 809-811 ◽

Cited By ~ 3

Author(s):

Brielle V. Rosa ◽

Hugh T. Blair ◽

Mark H. Vickers ◽

Cameron G. Knight ◽

Patrick C. H. Morel ◽

...

Keyword(s):

Estrous Cycle ◽

Undercarboxylated Osteocalcin ◽

Serum Concentrations ◽

Sprague Dawley ◽

Sprague Dawley Rats

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Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.4.1828 ◽

2001 ◽

Vol 91 (4) ◽

pp. 1828-1835 ◽

Cited By ~ 60

Author(s):

Nicole Stupka ◽

Peter M. Tiidus

Keyword(s):

Muscle Damage ◽

Ischemia Reperfusion Injury ◽

Serum Insulin ◽

Ischemia Reperfusion ◽

Neutrophil Infiltration ◽

Female Rats ◽

Protective Effects ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

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Infarct size is increased in female post-MI rats treated with rapamycin

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y09-031 ◽

2009 ◽

Vol 87 (6) ◽

pp. 460-470 ◽

Cited By ~ 6

Author(s):

Claude Lajoie ◽

Viviane El-Helou ◽

Cindy Proulx ◽

Robert Clément ◽

Hugues Gosselin ◽

...

Keyword(s):

Left Ventricle ◽

Female Rats ◽

Coronary Artery Ligation ◽

Female Rat ◽

Sprague Dawley ◽

Ischemic Insult ◽

Fibrotic Response ◽

Artery Ligation ◽

Sprague Dawley Rats ◽

Scar Healing

Rapamycin represents a recognized drug-based therapeutic approach to treat cardiovascular disease. However, at least in the female heart, rapamycin may suppress the recruitment of putative signalling events conferring cardioprotection. The present study tested the hypothesis that rapamycin-sensitive signalling events contributed to the cardioprotective phenotype of the female rat heart after an ischemic insult. Rapamycin (1.5 mg/kg) was administered to adult female Sprague–Dawley rats 24 h after complete coronary artery ligation and continued for 6 days. Rapamycin abrogated p70S6K phosphorylation in the left ventricle of sham rats and the noninfarcted left ventricle (NILV) of 1-week postmyocardial-infarcted (MI) rats. Scar weight (MI 0.028 ± 0.006, MI+rapamycin 0.064 ± 0.004 g) and surface area (MI 0.37 ± 0.08, MI+rapamycin 0.74 ± 0.03 cm2) were significantly larger in rapamycin-treated post-MI rats. In the NILV of post-MI female rats, rapamycin inhibited the upregulation of eNOS. Furthermore, the increased expression of collagen and TGF-β3 mRNAs in the NILV were attenuated in rapamycin-treated post-MI rats, whereas scar healing was unaffected. The present study has demonstrated that rapamycin-sensitive signalling events were implicated in scar formation and reactive fibrosis. Rapamycin-mediated suppression of eNOS and TGF-β3 mRNA in post-MI female rats may have directly contributed to the larger infarct and attenuation of the reactive fibrotic response, respectively.

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The cartilage degeneration in a growing rat experimental model of developmental trochlear dysplasia is associated with activation of PI3K/AKT signal pathway

10.21203/rs.3.rs-24905/v1 ◽

2020 ◽

Author(s):

Wei Lin ◽

Yike Dai ◽

Jinghui Niu ◽

Chongyi Fan ◽

Xunkai Feng ◽

...

Keyword(s):

Trochlear Dysplasia ◽

Cartilage Degeneration ◽

Signal Pathway ◽

Control Group ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Growing Rat ◽

Polymerase Chain ◽

Underlying Mechanisms ◽

Experimental Group

Abstract Background As one of the lower extremity deformities in human, trochlear dysplasia is a commonly encountered disease. However, the molecular mechanism of cartilage degeneration in trochlear dysplasia is indefinite yet. It was apparent to all that PI3K/AKT signal pathway is extremely significant in regulating the pathophysiological process of cartilage degeneration. The purpose of this research is to discuss the correlation between PI3K/AKT signal pathway and trochlear dysplasia cartilage degeneration. Materials and methods 120 female Sprague-Dawley rats at 4 weeks of age were separate into control group and experimental group randomly. The distal femurs were isolated from the experimental and unsurgeried control group at the point of the 4, 8, 12 weeks, correspondingly. Micro-CT and histological examination were carried out to investigate the anatomical structure and cartilage changes of the trochlear. Subsequently, the expression of PI3K/AKT, TGFβ1 and ADAMTS-4 in cartilage were investigated by immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). Results In the experimental group, the trochlear dysplasia model was successfully established at 8 weeks after surgery. Moreover, the cartilage degeneration was found from 8 weeks, with continued higher protein and mRNA expression of PI3K/AKT, TGFβ1 and ADAMTS-4 compared with the control group. Conclusions This research suggested that patellar instability may lead to trochlear dysplasia in growing rats. Moreover, trochlear dysplasia was probably one of the causes of patellofemoral osteoarthritis and the cartilage degeneration in trochlear dysplasia might be associate with activation of PI3K/AKT signal pathway. However, more research was required to clarify the underlying mechanisms.

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Hypertensive female Sprague-Dawley rats require an intact nitric oxide synthase system for compensatory increases in renal regulatory T cells

AJP Renal Physiology ◽

10.1152/ajprenal.00228.2020 ◽

2020 ◽

Vol 319 (2) ◽

pp. F192-F201

Author(s):

Lindsey A. Ramirez ◽

Ellen E. Gillis ◽

Jacqueline B. Musall ◽

Riyaz Mohamed ◽

Elizabeth Snyder ◽

...

Keyword(s):

Nitric Oxide ◽

T Cells ◽

Angiotensin Ii ◽

Nitric Oxide Synthase ◽

Regulatory T Cells ◽

Female Rats ◽

Sprague Dawley ◽

Albumin Excretion ◽

Sprague Dawley Rats ◽

Oxide Synthase

We have previously shown that hypertensive female rats have more regulatory T cells (Tregs), which contribute more to blood pressure (BP) control in female versus male rats. Based on known protective properties of Tregs, the goal of the present study was to investigate the mechanisms by which female rats maintain Tregs. The present study was designed to 1) compare the impact of three hypertension models on the percentage of renal Tregs and 2) test the hypothesis that nitric oxide synthase (NOS) inhibition prevents increases in renal Tregs and exacerbates renal damage in female Sprague-Dawley rats. Rats (11–14 wk old) were randomized to one of the following four groups: control, norepinephrine (NE) infusion, angiotensin II infusion, or the NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) in drinking water. BP was measured via tail cuff. After 2 wk of treatment, kidneys were isolated and processed to measure Tregs via flow cytometric analysis and renal injury via urinary albumin excretion, plasma creatinine, and histological analyses. Hypertensive treatments increased BP in all experimental animals. Increases in BP in norepinephrine-and angiotensin II-treated rats were associated with increases in renal Tregs versus control. In contrast, l-NAME treatment decreased Tregs compared with all groups. l-NAME treatment modestly increased albumin excretion. However, plasma creatinine was comparable among the groups, and there was no histological evidence of glomerular or tubular injury. This study provides insights into the mechanisms regulating renal Tregs and supports that an intact NOS system is crucial for female rats to have BP-related increases in renal Tregs.

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Impaired follicular development and endocrine disorders in female rats by prepubertal exposure to toxic doses of cadmium

Toxicology and Industrial Health ◽

10.1177/0748233720912060 ◽

2020 ◽

Vol 36 (2) ◽

pp. 63-75

Author(s):

Saman Saedi ◽

Mohammad Reza Jafarzadeh Shirazi ◽

Mohammad Javad Zamiri ◽

Mehdi Totonchi ◽

Mohammad Dadpasand ◽

...

Keyword(s):

Steroid Hormones ◽

Endocrine System ◽

Follicular Development ◽

Female Rats ◽

High Dose ◽

Endocrine Disorders ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Puberty Onset ◽

Different Doses

Cadmium (Cd) has been associated with several physiological problems including reproductive and endocrine system dysfunction resulting in temporary infertility. The principal objective of this project was to investigate the effects of prepubertal exposure to toxic doses of Cd on puberty onset, the endocrine system, and follicular development. For this purpose, 16 female Sprague-Dawley rats weaned on postnatal day (PND) 21 were randomly divided into 4 groups ( n = 4 per group). The treatments were as follows: 0, 25, 50, and 75 mg/kg/day of cadmium chloride (CdCl2) by oral gavage from PND 21 to observation of first vaginal opening (VO). The results demonstrated that prepubertal exposure to different doses of CdCl2 delays the age of VO, first diestrus, and first proestrus via altering the concentrations of estradiol and progesterone. The low level of these steroid hormones contributed to lower differentiation and maturation of follicles and it finally led to reduced ovarian reservoir of follicles and impaired follicular development. The number of atretic follicles and secondary follicles with premature cavity increased in rats that received a high dose of CdCl2, whereas the number of secondary follicles and corpora luteum decreased in the same circumstances. Taken together, these data suggest that prepubertal exposure to toxic doses of Cd delays the onset of puberty via disorderliness in the concentration of steroid hormones and reduces the ovarian reservoir of follicles, as well as folliculogenesis.

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Potency of Murraya koenigii Leaves as Anti-Cancer Mammary in 7,12 dimethylbenz(α) anthracene (DMBA) induced-Sprague Dawley Rats

E3S Web of Conferences ◽

10.1051/e3sconf/202015101058 ◽

2020 ◽

Vol 151 ◽

pp. 01058

Author(s):

Siti Aisyah ◽

Ekowati Handharyani ◽

Nurliani Bermawie ◽

Agus Setiyono

Keyword(s):

Mammary Tumor ◽

Tumor Size ◽

Histopathological Examination ◽

Tumor Development ◽

Collagen Fibers ◽

Female Rats ◽

Sprague Dawley ◽

Murraya Koenigii ◽

Sprague Dawley Rat ◽

Sprague Dawley Rats

The purpose of the research was to study the potency of Murraya koenigii leaves extract to overcome the mammary tumor in Sprague Dawley rat. Thirty-five female rats were divided into seven groups: control (P1), tumor without therapy (P2), methotrexate group (P3), curative groups (P4 and P5) were given extract after the tumor was formed, and preventive groups (P6 and P7) were given extract before the tumor was formed with dose of 300 and 400 mg/kg, respectively. The induction of mammary tumor in rats were carried out using 7,12 dimethylbenz(α) anthracene (DMBA) subcutaneously. Bodyweight and tumor size were measured every week for 4 weeks. At the end of treatment, rats were euthanized and mammary glands were collected for histopathological examination. The result showed tumor size in P2 was significantly higher (p<0.05) than in other groups. On the other hand, tumor size in P4 and P6 were significantly smaller (p<0.05) compared to P5 and P7. Histopathological changes showed PMN cells, 1-3 layers of cuboid epithelial and solid collagen fibers proliferation in P2, while in P3 to P7 showed moderate collagen fibers proliferation. In conclusion, the administration of the extract at a dose of 300 mg/kg can decelerate tumor development in Sprague Dawley rat mammary gland.

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Subchronic Toxicity of S-111-S-WB in Sprague Dawley Rats

International Journal of Toxicology ◽

10.1177/1091581810370372 ◽

2010 ◽

Vol 29 (4) ◽

pp. 358-371 ◽

Cited By ~ 6

Author(s):

Jozef J. W. M. Mertens ◽

Daniel W. Sved ◽

Gary B. Marit ◽

Nichole R. Myers ◽

Phil L. Stetson ◽

...

Keyword(s):

Alkaline Phosphatase ◽

Steady State ◽

Ammonium Salts ◽

Serum Concentrations ◽

Sprague Dawley ◽

Subchronic Toxicity ◽

Lower Serum ◽

Sprague Dawley Rats ◽

Steady State Serum ◽

Effect Level

S-111-S-WB, a mixture of perfluoro fatty acid ammonium salts (C6-C13), was administered orally to Crl:CD (SD)IGS-BR rats. Higher hepatic β-oxidation and liver weights with hepatocellular hypertrophy were present at the 0.125 and 0.6 mg/kg/d dosage. The 0.6 mg/kg/d males developed hepatocellular degeneration and necrosis. Lower serum protein and higher bilirubin and BUN were seen in the 0.6 mg/kg/d males and lower globulin and higher alkaline phosphatase in the 0.125 mg/kg/d males and 0.6 mg/kg/d animals. After 2 weeks, serum concentrations of pentadecafluorooctanoic acid (C8), heptadecafluorononanoic acid (C9), perfluoroundecanoic acid (C11), and perfluorotridecanoic acid (C13) were constant for at least 8 hours. After 90 days, only C9 in the 0.025 mg/kg/d females had reached steady state. Serum C8 and C9 concentrations in the males were 10-fold higher than in the females, whereas C11 and C13 were similar for both genders. The main elimination was via the urine for C8 (males) and C9 (females), and via the feces for C11 and C13. The no-observed-effect level (NOEL) was 0.025 mg/kg/d for the males and 0.125 mg/kg/d for the females.

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A novel 4 S [3H]β-naphthoflavone-binding protein in liver cytosol of female Sprague–Dawley rats treated with aryl hydrocarbon receptor agonists

Biochemical Journal ◽

10.1042/bj3470787 ◽

2000 ◽

Vol 347 (3) ◽

pp. 787-795

Author(s):

Damian BRAUZE ◽

Danuta MALEJKA-GIGANTI

Keyword(s):

Aryl Hydrocarbon Receptor ◽

Rat Liver ◽

Binding Protein ◽

Female Rats ◽

Sprague Dawley ◽

Methyltransferase Activity ◽

Liver Cytosol ◽

Aryl Hydrocarbon ◽

Sprague Dawley Rats ◽

S Peak

β-Naphthoflavone (β-NF) is a widely used inducer of phase-I and phase-II enzymes controlled by aryl hydrocarbon receptor (AhR). Studies of competitive binding with 3H-labelled 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3-MC) and benzo[a]pyrene (B[a]P) have shown that β-NF is a high-affinity ligand for AhR and also for polycyclic aromatic hydrocarbon (PAH)-binding protein, both soluble proteins of rat liver in 8 S and 4 S fractions, respectively, of sucrose gradients. This study examined binding of [3H]β-NF to liver cytosolic proteins of female Sprague-Dawley rats. Treatment of rats with β-NF, 3-MC, TCDD or α-naphthoflavone (α-NF) increased the specific [3H]β-NF binding to liver cytosol up to 125-fold that of vehicle (corn oil)-treated rats (< 100 fmol/mg of protein). Sucrose gradients revealed a large 4 S and a small 8 S peak of radioactivity from [3H]β-NF binding to cytosols of β-NF-, 3-MC-, TCDD- or α-NF-treated rats. Whereas co-incubation with the unlabelled β-NF eliminated both peaks, co-incubation with 2,3,7,8-tetrachlorodibenzofuran (TCDF) eliminated only the 8 S peak. The sucrose density gradient from [3H]TCDD binding to cytosol of β-NF- or TCDD-treated rats yielded a small 4 S and a larger 8 S peak; only the latter was abolished by co-incubation with TCDF. Thus, the patterns of sedimentation, distribution and elimination of radioactivity from the 8 S fraction of the liver cytosols from β-NF-, 3-MC-, TCDD- or α-NF-treated rats were characteristic for the AhR, whereas those from the 4 S fraction appeared specific for [3H]β-NF binding. The data indicate that potent AhR agonists, TCDD, 3-MC and β-NF, and to a lesser extent α-NF, a weak AhR agonist, induce a 4 S [3H]β-NF-binding protein in liver cytosol of female rats. α-NF, β-NF and 3-MC were effective competitors (80-85% inhibition) of the [3H]β-NF-specific binding to the β-NF-, 3 MC- or TCDD-induced 4 S protein, whereas several PAHs including B[a]P and benzo[e]pyrene were only weak competitors. The increased [3H]β-NF binding was not associated with glycine N-methyltransferase activity. Hence, the 4 S [3H]β-NF-binding protein described herein differs from the constitutive 4 S PAH-binding protein of rat liver cytosols in the inducibility by β-NF and 3-MC, ligand-binding characteristics, and lack of glycine N-methyltransferase activity. Gel filtration on Sephacryl of liver cytosols from β-NF-treated rats indicated a molecular mass of ≈ 42 kDa for [3H]β-NF-bound protein and suggested that it was derived from a large mass component that before the radioligand binding was eluted with the void volume of the gel and sedimented in a 7 S fraction of the sucrose gradient. The [3H]β-NF binding activity was not eluted with glutathione S-transferase Ya, aldehyde-3-dehydrogenase or DT-diaphorase [NAD(P)H: quinone oxidoreductase] activities, which are AhR-controlled and β-NF-inducible. Further studies are needed to determine the identity and function of this novel protein which may be involved either directly or indirectly (as a carrier protein) in xenobiotic metabolism in vivo.

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