EFFECT OF BU-ZHONG-YI-QI-TANG ON SEMINAL PLASMA CYTOKINE LEVELS IN PATIENTS WITH IDIOPATHIC MALE INFERTILITY

2004 ◽  
Vol 50 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Y. FURUYA ◽  
T. AKASHI ◽  
H. FUSE
2020 ◽  
Vol 21 (19) ◽  
pp. 7308 ◽  
Author(s):  
Rossella Cannarella ◽  
Federica Barbagallo ◽  
Andrea Crafa ◽  
Sandro La Vignera ◽  
Rosita A. Condorelli ◽  
...  

As the “-omic” technology has largely developed, its application in the field of medical science seems a highly promising tool to clarify the etiology, at least in part, of the so-called idiopathic male infertility. The seminal plasma (SP) is made-up of secretions coming from the male accessory glands, namely epididymis, seminal vesicles, and prostate. It is not only a medium for sperm transport since it is able to modulate the female reproductive environment and immunity, to allow the acquisition of sperm competence, to influence the sperm RNA content, and even embryo development. The aim of this systematic review was to provide an updated and comprehensive description of the main transcripts and proteins reported by transcriptome and proteome studies performed in the human SP of patients with idiopathic infertility, in the attempt of identifying possible candidate molecular targets. We recurrently found that micro RNA (miR)-34, miR-122, and miR-509 are down-regulated in patients with non-obstructive azoospermia (NOA) and oligozoospermia compared with fertile controls. These molecules may represent interesting targets whose predictive role in testicular sperm extraction (TESE) or assisted reproductive techniques (ART) outcome deserves further investigation. Furthermore, according to the available proteomic studies, ECM1, TEX101, lectingalactoside-binding andsoluble 3 binding protein (LGALS3BP) have been reported as accurate predictors of TESE outcome. Interestingly, ECM1 is differently expressed in patients with different ART outcomes. Further prospective, ample-sized studies are needed to validate these molecular targets that will help in the counseling of patients with NOA or undergoing ART.


2021 ◽  
Author(s):  
Danielle A. Simmons ◽  
Brian D. Mills ◽  
Robert R. Butler III ◽  
Jason Kuan ◽  
Tyne L. M. McHugh ◽  
...  

AbstractHuntington’s disease (HD) is caused by an expansion of the CAG repeat in the huntingtin gene leading to preferential neurodegeneration of the striatum. Disease-modifying treatments are not yet available to HD patients and their development would be facilitated by translatable pharmacodynamic biomarkers. Multi-modal magnetic resonance imaging (MRI) and plasma cytokines have been suggested as disease onset/progression biomarkers, but their ability to detect treatment efficacy is understudied. This study used the R6/2 mouse model of HD to assess if structural neuroimaging and biofluid assays can detect treatment response using as a prototype the small molecule p75NTR ligand LM11A-31, shown previously to reduce HD phenotypes in these mice. LM11A-31 alleviated volume reductions in multiple brain regions, including striatum, of vehicle-treated R6/2 mice relative to wild-types (WTs), as assessed with in vivo MRI. LM11A-31 also normalized changes in diffusion tensor imaging (DTI) metrics and diminished increases in certain plasma cytokine levels, including tumor necrosis factor-alpha and interleukin-6, in R6/2 mice. Finally, R6/2-vehicle mice had increased urinary levels of the p75NTR extracellular domain (ecd), a cleavage product released with pro-apoptotic ligand binding that detects the progression of other neurodegenerative diseases; LM11A-31 reduced this increase. These results are the first to show that urinary p75NTR-ecd levels are elevated in an HD mouse model and can be used to detect therapeutic effects. These data also indicate that multi-modal MRI and plasma cytokine levels may be effective pharmacodynamic biomarkers and that using combinations of these markers would be a viable and powerful option for clinical trials.


2021 ◽  
Vol 53 (3) ◽  
pp. 407-421
Author(s):  
Jaewoong Jang ◽  
Jaewon Song ◽  
Hyunji Lee ◽  
Inae Sim ◽  
Young V. Kwon ◽  
...  

AbstractEndotoxemia, a type of sepsis caused by gram-negative bacterial endotoxin [i.e., lipopolysaccharide (LPS)], is associated with manifestations such as cytokine storm; failure of multiple organs, including the liver; and a high mortality rate. We investigated the effect and mechanism of action of LGK974, a Wnt signaling inhibitor, in mice with LPS-induced endotoxemia, an animal model of sepsis. LGK974 significantly and dose-dependently increased the survival rate and reduced plasma cytokine levels in mice with LPS-induced endotoxemia. Transcriptome analysis of liver tissues revealed significant changes in the expression of genes associated with the Wnt pathway as well as cytokine and NF-κB signaling during endotoxemia. LGK974 treatment suppressed the activation of NF-κB signaling and cytokine expression as well as the Wnt/β-catenin pathway in the livers of endotoxemic mice. Coimmunoprecipitation of phospho-IκB and β-transducin repeat-containing protein (β-TrCP) was increased in the livers of endotoxemic mice but was reduced by LGK974 treatment. Moreover, LGK974 treatment decreased the coimmunoprecipitation and colocalization of β-catenin and NF-κB, which were elevated in the livers of endotoxemic mice. Our results reveal crosstalk between the Wnt/β-catenin and NF-κB pathways via interactions between β-TrCP and phospho-IκB and between β-catenin and NF-κB during endotoxemia. The results of this study strongly suggest that the crosstalk between the Wnt/β-catenin and NF-κB pathways contributes to the mutual activation of these two pathways during endotoxemia, which results in amplified cytokine production, liver damage and death, and that LGK974 suppresses this vicious amplification cycle by reducing the crosstalk between these two pathways.


2009 ◽  
Vol 52 (4) ◽  
pp. 493-497 ◽  
Author(s):  
Judith M Haissman ◽  
Lasse S Vestergaard ◽  
Samuel Sembuche ◽  
Christian Erikstrup ◽  
Bruno Mmbando ◽  
...  

2013 ◽  
Vol 4 (2) ◽  
pp. 20-25
Author(s):  
ZU Naher ◽  
SK Biswas ◽  
FH Mollah ◽  
M Ali ◽  
MI Arslan

Infertility is a worldwide problem and in almost 50% of cases infertility results from abnormality of the male partners. Apart from endocrine disorders, definitive cause and mechanism of male infertility is not clear in many cases. Recent evidence indicates that imbalance between pro-oxidant stress and antioxidant defense plays an important role in the pathogenesis of male infertility. Among the endogenous antioxidant systems, reduced glutathione (GSH) plays a significant role in the antioxidant defense of the spermatogenic epithelium, the epididymis and perhaps in the ejaculated spermatozoa. The current study was therefore designed to evaluate any association that may exist between GSH levels and male infertility. Infertile male patients (having female partners with normal fertility parameters; n=31) and age- matched healthy male fertile control subjects (n=30) were included in this study. In addition to medical history, semen analyses including semen volume, sperm count, motility and morphology were done for each subject. As a measure of antioxidant capacity erythrocyte and seminal plasma GSH concentrations were measured by Ellman's method in fertile and infertile male subjects. The infertile subjects were similar to fertile subjects in terms of age. However, semen volume and sperm count was found significantly lower (p<0.001) in infertile males compared with healthy fertile male subjects. Percentage of subjects with abnormal sperm morphology and motility were found higher in infertile group compared with fertile group. The median (range) erythrocyte GSH level did not differ between the two groups (12.62 (0.67-29.82) versus 13.93 (2.10-21.08) mg/gm Hb). However, the seminal plasma GSH level was found markedly suppressed in infertile group (1.64 (0.23-7.50)) compared with fertile group (4.26 (2.32-7.50)) mg/dl (p<0.001). In the present study seminal plasma GSH level was found markedly suppressed along with abnormal values for semen volume, sperm concentration and sperm morphology and motility in infertile subjects compared with fertile subjects. This finding indicates that low level of seminal plasma GSH level may be associated with male infertility. DOI: http://dx.doi.org/10.3329/bjmb.v4i2.13772 Bangladesh J Med Biochem 2011; 4(2): 20-25


2014 ◽  
Vol 86 (3) ◽  
pp. 164 ◽  
Author(s):  
Davide Arcaniolo ◽  
Vincenzo Favilla ◽  
Daniele Tiscione ◽  
Francesca Pisano ◽  
Giorgio Bozzini ◽  
...  

Objective: Infertility affects 15% of couples in fertile age. Male factor is a cause of infertility in almost half of cases, mainly due to oligoasthenoteratozoospermia (OAT). The purpose of this study is to review the effects of nutritional supplements as medical treatment for idiopathic male infertility. Material and methods: A Pub Med and Medline review of the published studies utilizing nutritional supplements for the treatment of male infertility has been performed. Results: Clinical trials on Vitamin E, Vitamin A, Vitamin C. Arginine, Carnitine, N-Acetyl-Carnitine, Glutathione, Coenzyme Q10, Selenium and Zinc were reviewed. Although there is a wide variability in selected population, dose regimen and final outcomes, nutritional supplements both alone and in combination seems to be able to improve semen parameters (sperm count, sperm motility and morphology) and pregnancy rate in infertile men. Conclusions: There are rising evidences from published randomized trials and systematic review suggesting that nutritional supplementation may improve semen parameters and the likelihood of pregnancy in men affected by OAT. This improvement, however, is not consistent and there is a wide variation in the treatment regimens used. Well designed and adequately powered RCTs are needed to better clarify the role of nutritional supplements as treatment for male infertility.


2016 ◽  
Vol 5 (4) ◽  
pp. 369-377 ◽  
Author(s):  
Jos A. Bouwens ◽  
Erik van Duijn ◽  
Christa M. Cobbaert ◽  
Raymund A.C. Roos ◽  
Roos C. van der Mast ◽  
...  

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