Soleus muscle force following downhill running in ovariectomized rats treated with estrogen

2006 ◽  
Vol 31 (4) ◽  
pp. 449-459 ◽  
Author(s):  
Sofia Sotiriadou ◽  
Antonios Kyparos ◽  
Maria Albani ◽  
Georgios Arsos ◽  
Mark S.F. Clarke ◽  
...  
Keyword(s):  
Soleus Muscle ◽  
Muscle Injury ◽  
Ovariectomized Rats ◽  
Tetanic Force ◽  
Downhill Running ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
Maximal Tetanic Force ◽  
40 Hz

The ovariectomized (OVX) rat model was used to investigate the effects of estrogen treatment on soleus muscle functionality in situ following muscle injury induced by downhill running. Fifty immature, 24- to 26-d-old, OVX rats were randomly assigned to 5 separate experimental groups: sedentary controls (OVX-Sed), placebo-treated and studied immediately after exercise (OVX-Pb0), placebo-treated and studied 72 h after exercise (OVX-Pb72), estradiol-treated and studied immediately after exercise (OVX-Ed0), and estradiol-treated and studied 72 h after exercise (OVX-Ed72). At the age of 9 weeks, under ketamine and xylazine anesthesia i.p., the rats were subcutaneously implanted with either placebo or 17β-estradiol-impregnated pellets (0.05 mg/pellet, 3 week release). Treatment with 17β-estradiol increased the estradiol plasma levels in OVX animals to those normally seen during the proestrous cycle of normal animals. Three weeks after the implantation the rats were subjected to a 90 min intermittent downhill running protocol. Our results indicate that the exercise protocol used in the study induced injury in the soleus muscle, as it was detected by the significant reduction in unfused (stimulation at 10, 20, and 40 Hz) and maximal (Po) tetanic force, as well as the decreased ability of the soleus muscle to maintain tension (stimulation at 40 Hz for 3 min) in OVX-Pb0 and OVX-Pb72 placebo-treated animals subjected to downhill running (injured muscles) as compared with OVX-Sed control rats (uninjured muscle). Estradiol replacement in OVX rats partially protected the soleus muscle from the injury normally induced by downhill running. As compared with the OVX-Pb0 and OVX-Pb72 placebo-treated groups, the soleus muscles of OVX-Ed0 and OVX-Ed72 estradiol-treated rats were capable of producing significantly greater unfused tetanic force and had an increased ability to maintain tension after fatigue. However, estrogen at the dose administered did not prevent the decrease in maximal tetanic force. We postulate that the protective effect of estrogens on muscle strength may be related to the ability of estrogen hormones to attenuate the E–C coupling failure and (or) the disorganization of the contractile apparatus associated with eccentric exercise through a mechanism or mechanisms yet to be fully understood.

A Decrease in Soleus Muscle Force Generation in Rats After Downhill Running

2001 ◽  
Vol 26 (4) ◽  
pp. 323-335 ◽  
Author(s):  
Antonios Kyparos ◽  
Chrysoula Matziari ◽  
Maria Albani ◽  
Georgios Arsos ◽  
Sofia Sotiriadou ◽  
...  
Keyword(s):  
Soleus Muscle ◽  
Muscle Injury ◽  
Low Frequency ◽  
Eccentric Contraction ◽  
Contractile Properties ◽  
Tetanic Force ◽  
Time To Peak ◽  
Downhill Running ◽  
Male Wistar Rats ◽  
Isometric Twitch

The purpose of the present study was to investigate the immediate and 48-hr post-exercise effects of eccentric contraction-biased exercise on the contractile properties of the soleus muscle in situ. Adult male Wistar rats were categorised into sedentary control rats (n = 10), rats studied immediately (n = 10), and rats studied 48 hours after the exercise (n = 10). The exercise protocol consisted of a 90-min intermittent downhill running (-16°, 16 m/min) on a motor-driven treadmill. The contractile properties of the soleus muscle were recorded following i.p. chloral hydrate anaesthesia. Isometric twitch force (Pt), time-to-peak tension (TPT), half-relaxation time (1/2 RT), and tetanic force at stimulation frequencies of 40, 80, and 100 Hz were recorded. A low-frequency muscle fatigue protocol (stimulation at 4 Hz for 5 min) was applied to test for fatigability. The main findings indicated that Pt generation dropped both immediately and 48 hr after the exercise, while tetanic force was partially restored after 48 hr. Exercise-induced E-C coupling failure and contractile machinery disorganisation due to muscle injury are put forward as the main force reduction causes. Key words: eccentric exercise, muscle injury, SR, E-C coupling, tension recording

scholarly journals Estrogen and Estrogen Receptor-β (ERβ)-Selective Ligands Induce Galanin Expression within Gonadotropin Hormone-Releasing Hormone-Immunoreactive Neurons in the Female Rat Brain

Endocrinology ◽  
2005 ◽  
Vol 146 (6) ◽  
pp. 2760-2765 ◽  
Author(s):  
Istvan Merchenthaler ◽  
Gloria E. Hoffman ◽  
Malcolm V. Lane
Keyword(s):  
Ovariectomized Rats ◽  
Female Rat ◽  
Dependent Manner ◽  
Neuronal System ◽  
Selective Ligands ◽  
Gnrh Neurons ◽  
17Β Estradiol ◽  
Selective Agonists ◽  
The Many

Abstract Among the many factors that integrate the activity of the GnRH neuronal system, estrogens play the most important role. In females, estrogen, in addition to the negative feedback, also exhibits a positive feedback influence upon the activity and output of GnRH neurons to generate the preovulatory LH surge and ovulation. Until recently, the belief has been that the GnRH neurons do not contain estrogen receptors (ERs) and that the action of estrogen upon GnRH neurons is indirect involving several, estrogen-sensitive neurotransmitter and neuromodulator systems that trans-synaptically regulate the activity of the GnRH neurons. Based on our recent findings that GnRH neurons of the female rat coexpress galanin, that galanin is a potent GnRH-releasing peptide, and that ERβ is present in GnRH neurons, we have evaluated the effect of 17β-estradiol and two ERβ-selective agonists (WAY-200070, WAY-166818) on the expression of galanin within GnRH neurons. By combining immunocytochemistry for GnRH and in situ hybridization histochemistry for galanin, we demonstrate that 17β-estradiol (20 μg/kg, sc) stimulates galanin expression within GnRH-immunoreactive neurons in a time-dependent manner. A significant increase was observed 2 h after its administration to ovariectomized rats. However, a more robust expression required 3-d treatment regimen. Treatment with the β-selective ligands resulted in similar observations, although no statistical analysis is available for the 2 hr survival. These observations strongly suggest that estrogen and the ERβ-selective ligands stimulate galanin expression within GnRH neurons via ERβ, although an indirect mechanism via interneurons still cannot be ruled out.

scholarly journals Vitamin D and 17β-estradiol upregulate each other's receptors and regulating the AMPK/NF-κB pathway to relieve depressive-like behaviors in female ovariectomized rats

2019 ◽  
Author(s):  
Wen-yuan Zhang ◽  
Yujin Guo ◽  
Ke-yi Wang ◽  
Pei Jiang
Keyword(s):  
Vitamin D ◽  
Neuronal Damage ◽  
Chronic Administration ◽  
Ovariectomized Rats ◽  
Neuroprotective Effects ◽  
Ovx Rats ◽  
Increased Risk ◽  
17Β Estradiol ◽  
Induced Apoptosis ◽  
Control Sham

Abstract Background: A deficiency of vitamin D (VD) or 17β-estradiol (E2) is associated with increased risk of mood disorders such as depression in menopausal females, but the mechanism underlying is still elusive. The present study aims to evaluate whether vitamin D and 17β-estradiol could relieve a depressive-like state through neuroinflammatory regulation in ovariectomized (OVX) rats. Methods: Female SD rats were randomly divided into four groups, namely, control (SHAM), OVX, OVX+VD, and OVX+E2. The treatment procedure was performed for 10 weeks until sacrifice. Results: The chronic administration of vitamin D and 17β-estradiol showed anti-depressive-like activity in the OVX rats. Additionally, vitamin D and 17β-estradiol upregulated each other's receptors, including VDR, ERα, and ERβ in the hippocampus of OVX rats. Vitamin D and 17β-estradiol showed neuroprotective effects by decreasing OVX-induced apoptosis and neuronal damage, regulating the AMPK/NF-κB signaling pathway, and reducing the proinflammatory cytokines (IL-1β, IL-6, and TNFα), as well as iNOS and COX-2 in the hippocampus of OVX rats. Conclusions: The present study demonstrated that vitamin D and 17β-estradiol could upregulate each other's receptors and regulate the AMPK/NF-κB pathway to relieve the OVX-induced depressive-like state. The results should stimulate translational research towards the vitamin D potential for prevention or treatment of menopause-related depression.

Effects of 17β-estradiol and antioxidant administration on oxidative stress and insulin resistance in ovariectomized rats

2011 ◽  
Vol 89 (7) ◽  
pp. 497-504 ◽  
Author(s):  
Amr M. Abbas ◽  
Ayman Z. Elsamanoudy
Keyword(s):  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Vitamin E ◽  
Brain Cortex ◽  
Fasting Glucose ◽  
Ovariectomized Rats ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
The Brain

The prevalence of insulin resistance syndrome increases during menopause with the overproduction of reactive oxygen species and impairment of the free radical scavenger function. Therefore, we investigated the effects of 17β-estradiol (E2) and vitamin E, as an antioxidant, on lipid peroxidation and antioxidant levels in the brain cortex and liver of ovariectomized rats as well as on insulin resistance in those rats. Forty female Sprague–Dawley rats, 3 months of age and weighing 231.5 ± 9.4 g, were divided into 4 groups: sham, ovariectomized (OVX), OVX treated with E2 (40 µg/kg subcutaneously), and OVX treated with E2 and vitamin E (100 mg/kg intraperitoneally). The 4 groups received the appropriate treatment every day for 8 weeks. Levels of glutathione, glutathione peroxidase, superoxide dismutase , catalase, and malondialdehyde in the brain cortex and liver of ovariectomized rats were measured. Also, fasting plasma insulin, glucose, and homeostatis model assessment of insulin resistance (HOMA-IR) were determined. Malondialdehyde increased and antioxidants (glutathione, glutathione peroxidase, catalase, superoxide dismutase) decreased in the brain cortex and liver of OVX rats. Also, fasting glucose, insulin, and HOMA-IR increased in OVX rats. E2 and E2 plus vitamin E decreased malondialdehyde and increased antioxidants in the brain cortex and liver of OVX rats. Moreover, they decreased fasting glucose, insulin, and HOMA-IR in ovariectomized rats. This study demonstrates that E2 and E2 plus vitamin E supplementation to OVX rats may improve insulin resistance, strengthen the antioxidant system, and reduce lipid peroxidation.

scholarly journals Effects of SCH-23390 in Combination with a Low Dose of 17β-Estradiol on Anxiety-Like Behavior in Ovariectomized Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Julia Fedotova
Keyword(s):  
Dopamine Receptor ◽  
Low Dose ◽  
Sch 23390 ◽  
Skf 38393 ◽  
Ovariectomized Rats ◽  
Dopamine Receptor Agonist ◽  
Repeated Treatment ◽  
Black And White ◽  
Ovx Rats ◽  
17Β Estradiol

The aim of this study was to explore effects on anxiety-like behavior of D1dopamine receptor agonist, SKF-38393, and of D1dopamine receptor antagonist, SCH-23390, given alone or in combination with a low dose of 17β-estradiol (17β-E2) to ovariectomized (OVX) rats. Two weeks after surgery, OVX rats began 14 days of treatment with the vehicle, a low dose of 17β-E2(5.0 μg/rat, s.c.), SKF-38393 (0.1 mg/kg, i.p.), SCH-23390 (0.1 mg/kg, i.p.), SKF-38393 plus 17β-E2, or SCH-23390 plus 17β-E2. The animals were tested in the black and white model (BWM) and the open field test (OFT). SCH-23390 (0.1 mg/kg, i.p.) alone or in a combination with a low dose of 17β-E2(5.0 μg/rat, s.c.) resulted in anxiolytic-like effect in OVX rats in the BWM. Repeated treatment with SCH-23390 and 17β-E2profoundly increased anxiolytic-like effect of single substances exerted per se. Coadministration of SCH-23390 with 17β-E2increased frequency of rearing and grooming in OVX rats in OFT. SKF-38393 (0.1 mg/kg, i.p.) treatment failed to alter anxiety-like behavior in OVX rats in the BWM. The results of the present study suggest that 17β-E2and SCH-23390 interact to exert anxiolytic-like action and that each of these drugs can potentiate effects of each other.

scholarly journals 17β-Estradiol Exacerbated Experimental Occlusal Interference-Induced Chronic Masseter Hyperalgesia by Increasing the Neuronal Excitability and TRPV1 Function of Trigeminal Ganglion in Ovariectomized Rats

2021 ◽  
Vol 22 (13) ◽  
pp. 6945
Author(s):  
Yun Liu ◽  
Xiao-Xiang Xu ◽  
Ye Cao ◽  
Si-Yi Mo ◽  
Shan-Shan Bai ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Neuronal Excitability ◽  
Mechanical Hyperalgesia ◽  
Ovariectomized Rats ◽  
Facilitatory Effect ◽  
Transient Receptor Potential Vanilloid ◽  
Dependent Manner ◽  
Ovx Rats ◽  
17Β Estradiol

Pain symptoms in temporomandibular disorders (TMD) predominantly affect reproductive women, suggesting that estrogen regulates pain perception. However, how estrogen contributes to chronic TMD pain remains largely unclear. In the present study, we performed behavioral tests, electrophysiology, Western blot and immunofluorescence to investigate the role and underlying mechanisms of estrogen in dental experimental occlusal interference (EOI)-induced chronic masseter mechanical hyperalgesia in rats. We found that long-term 17β-estradiol (E2) replacement exacerbated EOI-induced masseter hyperalgesia in a dose-dependent manner in ovariectomized (OVX) rats. Whole-cell patch-clamp recordings demonstrated that E2 (100 nM) treatment enhanced the excitability of isolated trigeminal ganglion (TG) neurons in OVX and OVX EOI rats, and EOI increased the functional expression of transient receptor potential vanilloid-1 (TRPV1). In addition, E2 replacement upregulated the protein expression of TRPV1 in EOI-treated OVX rats. Importantly, intraganglionic administration of the TRPV1 antagonist AMG-9810 strongly attenuated the facilitatory effect of E2 on EOI-induced masseter mechanical sensitivity. These results demonstrate that E2 exacerbated EOI-induced chronic masseter mechanical hyperalgesia by increasing TG neuronal excitability and TRPV1 function. Our study helps to elucidate the E2 actions in chronic myogenic TMD pain and may provide new therapeutic targets for relieving estrogen-sensitive pain.

Rutin attenuates cerebral ischemia–reperfusion injury in ovariectomized rats via estrogen-receptor-mediated BDNF–TrkB and NGF–TrkA signaling

2018 ◽  
Vol 96 (5) ◽  
pp. 672-681 ◽  
Author(s):  
Hong Liu ◽  
Lili Zhong ◽  
Yuwei Zhang ◽  
Xuewei Liu ◽  
Ji Li
Keyword(s):  
Estrogen Receptor ◽  
Cerebral Ischemia ◽  
Body Mass ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ovariectomized Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Ovx Rats ◽  
Increased Risk ◽  
17Β Estradiol

Rutin, a flavonoid glycoside, has been reported to exert neuroprotective effects. Loss of endogenous estrogen and dysregulation of the estrogen receptor (ER) signaling pathway are associated with the increased risk of stroke in women after menopause. This study was performed to investigate whether rutin could protect against cerebral ischemia by modulating the ER pathway. Ovariectomized (OVX) rats were given intraperitoneal injections of vehicle (dimethyl sulfoxide), rutin (100 mg/kg body mass) or 17β-estradiol (100 μg/kg body mass) for 5 consecutive days. Then, the rats were subjected to middle cerebral artery occlusion (MCAO) for 1 h followed by a 24 h reperfusion to establish the cerebral ischemia–reperfusion (I/R) injury. We found that rutin improved the sensorimotor performance and recognition memory of rats subjected to I/R, decreased the infarct size, and attenuated neuron loss. Rutin treatment also increased the levels of ERα, ERβ, brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), tropomyosin receptor kinase A (TrkA), TrkB, and phospho-cAMP-responsive element binding protein (p-CREB) in rat hippocampus and cerebral cortex. The protective effects of rutin were comparable to that of 17β-estradiol, and were partially blocked by ICI182780, an ER antagonist. The above results suggest that rutin preconditioning ameliorates cerebral I/R injury in OVX rats through ER-mediated BDNF–TrkB and NGF–TrkA signaling.

scholarly journals Cumulative Effects Of Strontium Ranelate and Impact Exercise On Bone Mass In Ovariectomized Rats

2021 ◽  
Vol 22 (6) ◽  
pp. 3040
Author(s):  
Priscilla Aveline ◽  
Annabelle Cesaro ◽  
Marija Mazor ◽  
Thomas M. Best ◽  
Eric Lespessailles ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Fat Mass ◽  
Lipid Content ◽  
Strontium Ranelate ◽  
Bending Test ◽  
Ovariectomized Rats ◽  
Whole Body ◽  
Left Femur ◽  
Osteocyte Apoptosis ◽  
Ovx Rats

OBJECTIVE: To explore the effect of physical exercise (EXE), strontium ranelate (SR), or their combination on bone status in ovariectomized (OVX) rats. DESIGN: Sixty female Wistar rats were randomized to one of five groups: sham (Sh), OVX (O), OVX+EXE (OE), OVX+SR (OSR), and OVX+EXE+SR (OESR). Animals in EXE groups were subjected to 10 drops per day (45 cm in height); rats in SR groups received 625 mg/kg/day of SR, 5 days/week for 8 weeks. Bone mineral density (BMD) and bone mineral content (BMC, dual-energy X-ray absorptiometry (DXA)), mechanical strength of the left femur (three-point bending test), and femur microarchitecture of (micro-computed tomography imaging, microCT) analyses were performed to characterize biomechanical and trabecular/cortical structure. Bone remodeling, osteocyte apoptosis, and lipid content were evaluated by ELISA and immunofluorescence tests. RESULTS: In OVX rats, whole-body BMD, trabecular parameters, and osteocalcin (OCN) levels decreased, while weight, lean/fat mass, osteocyte apoptosis, and lipid content all increased. EXE after ovariectomy improved BMD and BMC, trabecular parameters, cross-sectional area (CSA), moment of inertia, and OCN levels while decreasing osteocyte apoptosis and lipid content. SR treatment increased BMD and BMC, trabecular parameters, CSA, stiffness, OCN, and alkaline phosphatase (ALP) levels. Furthermore, fat mass, N-telopeptide (NTX) level, osteocyte apoptosis, and lipid content significantly decreased. The combination of both EXE and SR improved bone parameters compared with EXE or SR alone. CONCLUSION: EXE and SR had positive and synergistic effects on bone formation and resorption.

scholarly journals Ultrasound Imaging Evaluation of Textural Features in Athletes with Soleus Pathology—A Novel Case-Control Study

2021 ◽  
Vol 18 (4) ◽  
pp. 1983 ◽  
Author(s):  
Blanca De-la-Cruz-Torres ◽  
Emmanuel Navarro-Flores ◽  
Daniel López-López ◽  
Carlos Romero-Morales
Keyword(s):  
Ultrasound Imaging ◽  
Soleus Muscle ◽  
Muscle Injury ◽  
Intraclass Correlation ◽  
Muscle Thickness ◽  
Tendon Injury ◽  
Muscle Injuries ◽  
Imaging Evaluation ◽  
Rater Reliability ◽  
Group A

Background: the aim of this study was to compare the echotexture of patients with soleus muscle injury and age matched controls. Methods: a sample of 62 athletes was recruited at the private clinic and was divided in two group: a healthy group (n = 31) and a soleus pathology group whose athletes had soleus muscle injury, located in the central tendon (n = 31). The muscle thickness (MTh), echointensity (EI) and echovariation (EV) were analyzed. An intra-rater reliability test (Intraclass Correlation Coefficient-ICC) was performed in order to analyze the reliability of the values of the measurements. Results: Sociodemographic variables did not show statistically significant differences (p > 0.05). Ultrasound imaging measurements who reported statistically significant differences were EI (p = 0.001) and standard deviation (SD) (p = 0.001). MTh and EV variables did not show statistically significant differences (p = 0.381 and p = 0.364, respectively). Moreover, reliability values for the MTh (ICC = 0.911), EI (ICC = 0.982), SD (ICC = 0.955) and EV (ICC = 0.963). Based on these results the intra-rater reliability was considered excellent. Conclusion: Athletes with a central tendon injury of soleus muscle showed a lower EI when they were compared to healthy athletes. The echogenicity showed by the quantitative ultrasound imaging measurement may be a more objective parameter for the diagnosis and follow-up the soleus muscle injuries.

scholarly journals Less Carcinogenic Chlorinated Estrogens Applicable to Hormone Replacement Therapy

2021 ◽  
Vol 22 (13) ◽  
pp. 7222
Author(s):  
Yoshinori Okamoto ◽  
Hideto Jinno ◽  
Shinji Itoh ◽  
Shinya Shibutani
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Metabolic Activation ◽  
Ovariectomized Rats ◽  
Estrogenic Potential ◽  
Carcinogenic Potential ◽  
Induced Tumors ◽  
Carcinogenic Effects ◽  
17Β Estradiol

Human estrogens prescribed for hormone replacement therapy (HRT) are known to be potent carcinogens. To find safer estrogens, several chlorinated estrogens were synthesized and their carcinogenic potential were determined. A pellet containing either 2-chloro-17β-estradiol (2-ClE2) or 4-chloro-17β-estradiol (4-ClE2) was implanted subcutaneously for 52 weeks into August Copenhagen Irish (ACI) rats, a preferred animal model for human breast cancer. 17β-Estradiol (E2) frequently induced mammary tumors while both 2-ClE2 and 4-ClE2 did not. Their 17α-ethinyl forms, thought to be orally active estrogens, were also synthesized. Neither 2-chloro-17α-ethinylestradiol (2-ClEE2) nor 4-chloro-17α-ethinylestradiol (4-ClEE2) induced tumors. The less carcinogenic effects were supported by histological examination of mammary glands of ACI rats treated with the chlorinated estrogens. A chlorine atom positioned at the 2- or 4-position of E2 may prevent the metabolic activation, resulting in reducing the carcinogenicity. 2-ClE2 and 4-ClE2 administered subcutaneously and 2-ClEE2 and 4-ClEE2 given orally to ovariectomized rats all showed uterotrophic potency, albeit slightly weaker than that of E2. Our results indicate that less carcinogenic chlorinated estrogens retaining estrogenic potential could be safer alternatives to the carcinogenic estrogens now in use for HRT.

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