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MOUSE ANTI DEHYDROEPIANDROSTERONE

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[#ABS11645] MOUSE ANTI DEHYDROEPIANDROSTERONE

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(1) Dehydroepiandrosterone supplementation combined with Weight-Loading Whole-Body Vibration Training (WWBV) affects exercise performance and muscle glycogen storage in middle-aged C57BL/6 mice.[TOP]

Pubmed ID :29725246
Publication Date : //
: Adequate nutritional intake and an optimal training program are important elements of any strategy to preserve or increase muscle mass and strength during aging. : In the current study, we investigate the effects of Dehydroepiandrosterone (DHEA), one of the most abundant circulating steroids in humans and a precursor hormone, supplementation combined with a weight-loading whole-body vibration (WWBV) on exercise performance, physical fatigue-related biochemical responses and testosterone content in middle-aged 9 months old C57BL/6 mice. : Male middle-aged C57BL/6 mice were divided into 3 groups (n = 8 per group) and treated for 4 weeks with the following: 1) Sedentary control (SC) with vehicle 2) DHEA supplementation (DHEA, 10.2 mg/kg) and 3) DHEA supplementation with WWBV training (DHEA: 10.2 mg/kg; WBV: 5.6 Hz, 2 mm, 0.13 g). Exercise performance was evaluated by forelimb grip strength and time to exhaustion, as well as changes in body composition and anti-fatigue levels after a 15-min swimming exercise. Fatigue-related biochemical responses of serum lactate, ammonia, glucose, creatine kinase (CK), and blood urea nitrogen (BUN) were measured following the swimming exercise. In addition, the biochemical parameters and the testosterone levels were measured at the end of the experiment. DHEA supplementation combined with WWBV training for 4 weeks significantly decreased the amount of white adipose tissue and increased the food and water intake. Additionally, WWBV+DHEA supplementation improved exercise performance, testosterone levels and glycogen contents of both liver and muscle. WWBV+DHEA supplementation also decreased serum lactate, ammonia and BUN levels, while increasing glucose levels following the 15-min swim test. Taken together, our results suggest that combining the WWBV training program with DHEA supplementation could provide an anti-fatigue pharmacological effect for elderly populations.

Authors : Chen Yi-Ming, Lee Hao-Chieh, Chen Mu-Tsung, Huang Chi-Chang, Chen Wen-Chyuan,



(2) Differential biological effects of dehydroepiandrosterone (DHEA) between mouse (B16F10) and human melanoma (BLM) cell lines.[TOP]

Pubmed ID :29484102
Publication Date : //
Dehydroepiandrosterone (DHEA) is a weak androgen and had been shown to have anti-cancer, anti-adipogenic and anti-inflammatory effects on mouse and other rodent models, but not on humans, suggesting a systemic level difference between mouse and human. Our previous study on DHEA biological functions involving a variety of cell lines, suggested that the functional differences between mouse and human existed even at the cellular level. Hence, using mouse and human melanoma cell models, effects of DHEA on cell growth, mechanism of cell death and mechanism of DHEA action were studied. Results indicated a differential biological effects of DHEA between mouse and human melanoma cell lines. These studies also suggested that the differential biological effects observed between these two cell lines could be due to the difference in the way DHEA was processed or metabolized inside the cell.

Authors : Joshi Kumud, Hassan Sherif S, Ramaraj Pandurangan,



(3) Protective effect of crocin against d-galactose-induced aging in mice.[TOP]

Pubmed ID :29387570
Publication Date : //
Aging is a multifactorial phenomenon, which attribute to different diseases and abnormalities in living systems. Oxidative stress, which is an important factor in aging, exacerbates this process via different mechanisms. Crocin (CR), one of the active components of saffron showed strong antioxidant effects. In the present study, anti-aging property of crocin was investigated in mice.

Authors : Mohammadi Elaheh, Mehri Soghra, Badie Bostan Hasan, Hosseinzadeh Hossein,



(4) Sigma-1 Receptor Agonists Induce Oxidative Stress in Mitochondria and Enhance Complex I Activity in Physiological Condition but Protect Against Pathological Oxidative Stress.[TOP]

Pubmed ID :29127580
Publication Date : //
The sigma receptor (σR) is a chaperone protein residing at mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), where it modulates Ca exchange between the ER and mitochondria by interacting with inositol-1,4,5 trisphosphate receptors (IPRs). The σR is highly expressed in the central nervous system and its activation stimulates neuromodulation and neuroprotection, for instance in Alzheimer's disease (AD) models in vitro and in vivo. σR effects on mitochondria pathophysiology and the downstream signaling are still not fully understood. We here evaluated the impacts of σR ligands in mouse mitochondria preparations on reactive oxygen species (ROS) production, mitochondrial respiration, and complex activities, in physiological condition and after direct application of amyloid Aβ peptide. σR agonists (2-(4-morpholinethyl)-1-phenylcyclohexanecarboxylate hydrochloride (PRE-084), tetrahydro-N,N-dimethyl-5,5-diphenyl-3-furanmethanamine (ANAVEX1-41, AN1-41), (S)-1-(2,8-dimethyl-1-thia-3,8-diazaspiro[4.5]dec-3-yl)-3-(1H-indol-3-yl)propan-1-one (ANAVEX3-71, AN3-71), dehydroepiandrosterone-3 sulfate (DHEA), donepezil) increased mitochondrial ROS in a σR antagonist-sensitive manner but decreased Aβ-induced increase in ROS. σR ligands (agonists or antagonists) did not impact respiration but attenuated Aβ-induced alteration. σR agonists (PRE-084, AN1-41, tetrahydro-N,N-dimethyl-2,2-diphenyl-3-furanmethanamine hydrochloride (ANAVEX2-73, AN2-73), AN3-71) increased complex I activity, in a Ca-dependent and σR antagonist-sensitive manner. σR ligands failed to affect complex II, III, and IV activities. The increase in complex I activity explain the σR-induced increase in ROS since ligands failed to affect other sources of ROS accumulation in mitochondria and homogenates, namely NADPH oxidase (NOX) and superoxide dismutase (SOD) activities. Furthermore, Aβ significantly decreased the activity of complexes I and IV and σR agonists attenuated the Aβ-induced complex I and IV dysfunctions. σR activity in mitochondria therefore results in a Ying-Yang effect, by triggering moderate ROS increase acting as a physiological signal and promoting a marked anti-oxidant effect in pathological (Aβ) conditions.

Authors : Goguadze Nino, Zhuravliova Elene, Morin Didier, Mikeladze Davit, Maurice Tangui,



(5) Studies on 16,17-Pyrazoline Substituted Heterosteroids as Anti-Alzheimer and Anti-Parkinsonian Agents Using LPS Induced Neuroinflammation Models of Mice and Rats.[TOP]

Pubmed ID :29019394
Publication Date : //
Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common forms of neurodegenerative disorders. Dehydroepiandrosterone (DHEA) has been reported as a neuroprotective steroid useful in the therapeutic management of neurodegenerative disorders such as AD and PD. Herein we report the synthesis and evaluation of a new series of 16,17-pyrazolinyl DHEA analogues 2-4a-d as neuroprotective agents using LPS-induced neuroinflammation animal models. Treatment with the pyrazoline substituted steroids considerably improved the LPS-induced learning, memory and movement deficits in animal models. Suppression of biochemical parameters of oxidative and nitrosative stress, acetylcholinesterase activity, and TNF-α levels was also observed. 16,17-Pyrazolinyl steroids 2c-4c substituted with a 4-pyridyl moiety at the 5-position of the heterocyclic ring were found to be the most potent agents and produced neuroprotective effects better than standard drugs celecoxib and dexamethasone. Of these pyrazoline substituted steroids, the N-acetyl analogue 3c displayed neuroprotective effects better than N-phenyl (4c), which in turn showed potency more than N-unsubstituted analogue 2c.

Authors : Singh Ranjit, Thota Sridhar, Bansal Ranju,



(6) DHEA increases epithelial markers and decreases mesenchymal proteins in breast cancer cells and reduces xenograft growth.[TOP]

Pubmed ID :28803991
Publication Date : //
Breast cancer is one of the most common neoplasias and the leading cause of cancer death in women worldwide. Its high mortality rate is linked to a great metastatic capacity associated with the epithelial-mesenchymal transition (EMT). During this process, a decrease in epithelial proteins expression and an increase of mesenchymal proteins are observed. On the other hand, it has been shown that dehydroepiandrosterone (DHEA), the most abundant steroid in human plasma, inhibits migration of breast cancer cells; however, the underlying mechanisms have not been elucidated. In this study, the in vitro effect of DHEA on the expression pattern of some EMT-related proteins, such as E-cadherin (epithelial), N-cadherin, vimentin and Snail (mesenchymal) was measured by Western blot and immunofluorescence in MDA-MB-231 breast cancer cells with invasive, metastatic and mesenchymal phenotype. Also, the in vivo effect of DHEA on xenograft tumor growth in nude mice (nu/nu) and on expression of the same epithelial and mesenchymal proteins in generated tumors was evaluated. We found that DHEA increased expression of E-cadherin and decreased N-cadherin, vimentin and Snail expression both in MD-MB-231 cells and in the formed tumors, possibly by DHEA-induced reversion of mesenchymal phenotype. These results were correlated with a tumor size reduction in mouse xenografts following DHEA administration either a week earlier or concurrent with breast cancer cells inoculation. In conclusion, DHEA could be useful in the treatment of breast cancer with mesenchymal phenotype.

Authors : Colín-Val Zaira, González-Puertos Viridiana Yazmín, Mendoza-Milla Criselda, Gómez Erika Olivia, Huesca-Gómez Claudia, López-Marure Rebeca,



(7) The effect of DHEA on apoptosis and cohesin levels in oocytes in aged mice.[TOP]

Pubmed ID :28717062
Publication Date : //
Female fertility declines with age as the number of ovarian follicles decreases and aneuploidy increases. Degradation of the cohesin complex might be responsible for age-related aneuploidy. Dehydroepiandrosterone (DHEA) can improve the ovarian reserve and reduce the rate of aneuploidy, but the relationship between DHEA and cohesin levels in oocytes is still unknown. The aim of the current study was to evaluate the effect of the supplement DHEA on ovarian function, including the number of follicles and cohesin levels in oocytes. C57BL/6J mice at 3 weeks, 6 weeks, 12 weeks, 6 months, and 10 months of age were used to obtain a systematic view into follicle apoptosis and cohesin levels in oocytes. Nine-month-old C57BL/6J mice were administered saline (n = 5), 17β-estradiol (100 µg/kg per day, n = 5), or DHEA (5mg/Kg per day, n = 5). After 4 weeks, aged mice were weighed and sacrificed, and ovarian tissue samples were prepared. Anti-VASA staining and HE staining were used to count the number of follicles. Anti-γHAX staining and TUNEL were used to measure follicle apoptosis and immunofluorescent staining was used to detect the levels of three oocyte cohesin subunits: REC8, SMC1β, and SMC3. Administration of the supplements 17β-estradiol and DHEA to aged mice increased the number of primordial and primary follicles and decreased the age-related apoptosis of follicles. Levels of the cohesin subunits REC8 and SMC1β declined with age, but DHEA and 17β-estradiol tended to delay that decline. The supplement DHEA increased the number of primordial and primary follicles in aged mice by inhibiting follicle apoptosis and tended to delay the decrease in cohesin levels in oocytes.

Authors : Chu Nan, Gui Yuyan, Qiu Xuemin, Zhang Na, Li Lisha, Li Dajin, Tang Wei, Gober Hans-Jürgen, Zhang Bin, Wang Ling,



(8) Suppressed oligodendrocyte steroidogenesis in multiple sclerosis: Implications for regulation of neuroinflammation.[TOP]

Pubmed ID :28707358
Publication Date : //
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Neurosteroids are reported to exert anti-inflammatory effects in several neurological disorders. We investigated the expression and actions of the neurosteroid, dehydroepiandrosterone (DHEA), and its more stable 3β-sulphated ester, DHEA-S, in MS and associated experimental models. CNS tissues from patients with MS and animals with experimental autoimmune encephalomyelitis (EAE) displayed reduced DHEA concentrations, accompanied by diminished expression of the DHEA-synthesizing enzyme CYP17A1 in oligodendrocytes (ODCs), in association with increased expression of inflammatory genes including interferon (IFN)-γ and interleukin (IL)-1β. CYP17A1 was expressed variably in different human neural cell types but IFN-γ exposure selectively reduced CYP17A1 detection in ODCs. DHEA-S treatment reduced IL-1β and -6 release from activated human myeloid cells with minimal effect on lymphocyte viability. Animals with EAE receiving DHEA-S treatment showed reduced Il1b and Ifng transcript levels in spinal cord compared to vehicle-treated animals with EAE. DHEA-S treatment also preserved myelin basic protein immunoreactivity and reduced axonal loss in animals with EAE, relative to vehicle-treated EAE animals. Neurobehavioral deficits were reduced in DHEA-S-treated EAE animals compared with vehicle-treated animals with EAE. Thus, CYP17A1 expression in ODCs and its product DHEA were downregulated in the CNS during inflammatory demyelination while DHEA-S provision suppressed neuroinflammation, demyelination, and axonal injury that was evident as improved neurobehavioral performance. These findings indicate that DHEA production is an immunoregulatory pathway within the CNS and its restoration represents a novel treatment approach for neuroinflammatory diseases.

Authors : Boghozian Roobina, McKenzie Brienne A, Saito Leina B, Mehta Ninad, Branton William G, Lu JianQiang, Baker Glen B, Noorbakhsh Farshid, Power Christopher,



(9) BNN-20, a synthetic microneurotrophin, strongly protects dopaminergic neurons in the "weaver" mouse, a genetic model of dopamine-denervation, acting through the TrkB neurotrophin receptor.[TOP]

Pubmed ID :28461162
Publication Date : //
Neurotrophic factors are among the most promising treatments aiming at slowing or stopping and even reversing Parkinson's disease (PD). However, in most cases, they cannot readily cross the human blood-brain-barrier (BBB). Herein, we propose as a therapeutic for PD the small molecule 17-beta-spiro-[5-androsten-17,2'-oxiran]-3beta-ol (BNN-20), a synthetic analogue of DHEA, which crosses the BBB and is deprived of endocrine side-effects. Using the "weaver" mouse, a genetic model of PD, which exhibits progressive dopaminergic neurodegeneration in the Substantia Nigra (SN), we have shown that long-term administration (P1-P21) of BNN-20 almost fully protected the dopaminergic neurons and their terminals, via i) a strong anti-apoptotic effect, probably mediated through the Tropomyosin receptor kinase B (TrkB) neurotrophin receptor's PI3K-Akt-NF-κB signaling pathway, ii) by exerting an efficient antioxidant effect, iii) by inducing significant anti-inflammatory activity and iv) by restoring Brain-Derived Neurotrophic Factor (BDNF) levels. By intercrossing "weaver" with NGL mice (dual GFP/luciferase-NF-κΒ reporter mice, NF-κΒ.GFP.Luc), we obtained Weaver/NGL mice that express the NF-κB reporter in all somatic cells. Acute BNN-20 administration to Weaver/NGL mice induced a strong NF-κB-dependent transcriptional response in the brain as detected by bioluminescence imaging, which was abolished by co-administration of the TrkB inhibitor ANA-12. This indicates that BNN-20 exerts its beneficial action (at least in part) through the TrkB-PI3K-Akt-NF-κB signaling pathway. These results could be of clinical relevance, as they suggest BNN-20 as an important neuroprotective agent acting through the TrkB neurotrophin receptor pathway, mimicking the action of the endogenous neurotrophin BDNF. Thus BNN-20 could be proposed for treatment of PD.

Authors : Botsakis Konstantinos, Mourtzi Theodora, Panagiotakopoulou Vasiliki, Vreka Malamati, Stathopoulos Georgios T, Pediaditakis Iosif, Charalampopoulos Ioannis, Gravanis Achilleas, Delis Foteini, Antoniou Katerina, Zisimopoulos Dimitrios, Georgiou Christos D, Panagopoulos Nikolaos T, Matsokis Nikolaos, Angelatou Fevronia,



(10) Modulation of steroidogenesis by vitamin D3 in granulosa cells of the mouse model of polycystic ovarian syndrome.[TOP]

Pubmed ID :28345956
Publication Date : //
Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder of women of reproductive age characterized by polycystic ovarian morphology, anovulation or oligomenorrhea, and hyperandrogenism. It is shown that disruption in the steroidogenesis pathway caused by excess androgen in PCOS is a critical element of abnormal folliculogenesis and failure in dominant follicle selection. Vitamin D plays an important role in the regulation of ovulatory dysfunction and can influence genes involved in steroidogenesis in granulosa cells. In the present study, we investigated the effects of vitamin D3 on steroidogenic enzyme expression and activities in granulosa cell using a PCOS mouse model. In our study, the PCOS mouse model was developed by the injection of dehydroepiandrosterone (DHEA) for 20 days. The mRNA and protein expression levels of genes involved in steroidogenesis in granulosa cells were compared between polycystic and normal ovaries using real-time PCR and Western blotting assays. Granulosa cells of DHEA-induced PCOS mice were then cultured with and without vitamin D3 and mRNA and protein expression levels of steroidogenic enzymes and serum 17beta-estradiol and progesterone levels were investigated using qRT-PCR, western blot, and radioimmunoassay, respectively. Steroidogenic enzymes including Cyp11a1, StAR, Cyp19a1, and 3β-HSD were upregulated in granulosa cells of PCOS mice when compared to normal mice. Treatment with vitamin D3 decreased mRNA and protein expression levels of steroidogenic enzymes in cultured granulosa cells. Vitamin D3 also decreased aromatase and 3β-HSD activity that leads to decreased 17beta-estradiol and progesterone release. This study suggests that vitamin D3 could modulate the steroidogenesis pathway in granulosa cells of PCOS mice that may lead to improving follicular development and maturation. This is a step towards a possible conceivable treatment for PCOS.

Authors : Bakhshalizadeh Shabnam, Amidi Fardin, Alleyassin Ashraf, Soleimani Masoud, Shirazi Reza, Shabani Nashtaei Maryam,