scholarly journals Pectinase-treated Panax ginseng protects heat stress-induced testicular damage in rats

Reproduction ◽  
2017 ◽  
Vol 153 (6) ◽  
pp. 737-747 ◽  
Author(s):  
Min Kyoung Kim ◽  
Kyu-Min Cha ◽  
Seock-Yeon Hwang ◽  
Un-Kyu Park ◽  
Seok Kyo Seo ◽  
...  

Testicular hyperthermia is well studied to cause impaired spermatogenesis. In the present study, the protective effect of enzymatically modified (pectinase-treated)Panax ginseng(GINST) against intermittent sub-chronic heat stress-induced testicular damage in rats was investigated. Male Sprague–Dawley rats were divided into four groups: normal control (NC), heat-stressed control (HC), heat-stressed plus GINST-100 mg/kg/day (HG100) and heat-stressed plus GINST-200 mg/kg/day (HG200) treatment groups. GINST (100 and 200 mg/kg/day) was mixed separately with a regular pellet diet and was administered orally for 8 weeks starting from 1 week before heat exposure. Parameters such as organ weight, blood chemistry, sperm kinetic values, expression of antioxidant enzymes, spermatogenesis molecules and sex hormone receptors levels were measured. Data revealed that kidney and epididymis weight were significantly (P < 0.05) decreased with heat stress and recovered by GINST treatment. Further, the altered levels of blood chemistry panels and sperm kinetic values in heat stress-induced rats were attenuated when GINST was administered (P < 0.05). Furthermore, the expression levels of antioxidant-related enzymes (GSTM5 and GPX4), spermatogenesis-related proteins (CREB1 and INHA) and sex hormone receptors (androgen receptor, luteinizing hormone receptor and follicle-stimulating hormone receptor) were reduced by heat stress; however, GINST treatment effectively ameliorated these changes. In conclusion, GINST was effective in reducing heat-induced damage in various male fertility factorsin vivoand has considerable potential to be developed as a useful supplement in improving male fertility.

2019 ◽  
Vol 43 (1) ◽  
pp. 135-142 ◽  
Author(s):  
Spandana Rajendra Kopalli ◽  
Kyu-Min Cha ◽  
Seock-Yeon Hwang ◽  
Min-Sik Jeong ◽  
Si-Kwan Kim

Author(s):  
C. Fede ◽  
G. Albertin ◽  
L. Petrelli ◽  
M.M. Sfriso ◽  
C. Biz ◽  
...  

Many epidemiologic, clinical, and experimental findings point to sex differences in myofascial pain in view of the fact that adult women tend to have more myofascial problems with respect to men. It is possible that one of the stimuli to sensitization of fascial nociceptors could come from hormonal factors such as estrogen and relaxin, that are involved in extracellular matrix and collagen remodeling and thus contribute to functions of myofascial tissue. Immunohistochemical and molecular investigations (real-time PCR analysis) of relaxin receptor 1 (RXFP1) and estrogen receptor-alpha (ERα) localization were carried out on sample of human fascia collected from 8 volunteers patients during orthopedic surgery (all females, between 42 and 70 yrs, divided into pre- and post-menopausal groups), and in fibroblasts isolated from deep fascia, to examine both protein and RNA expression levels. We can assume that the two sex hormone receptors analyzed are expressed in all the human fascial districts examined and in fascial fibroblasts culture cells, to a lesser degree in the post-menopausal with respect to the pre-menopausal women. Hormone receptor expression was concentrated in the fibroblasts, and RXFP1 was also evident in blood vessels and nerves. Our results are the first demonstrating that the fibroblasts located within different districts of the muscular fasciae express sex hormone receptors and can help to explain the link between hormonal factors and myofascial pain. It is known, in fact, that estrogen and relaxin play a key role in extracellular matrix remodeling by inhibiting fibrosis and inflammatory activities, both important factors affecting fascial stiffness and sensitization of fascial nociceptors.


2017 ◽  
Vol 41 (4) ◽  
pp. 578-588 ◽  
Author(s):  
Spandana Rajendra Kopalli ◽  
Kyu-Min Cha ◽  
Sang-Ho Lee ◽  
Ji-Hoon Ryu ◽  
Seock-Yeon Hwang ◽  
...  

1998 ◽  
Vol 20 (1) ◽  
pp. 119-127 ◽  
Author(s):  
TO Abney ◽  
J Zhai

Testicular Leydig cells (LC) are rapidly and selectively destroyed by an injection of ethane dimethane sulfonate (EDS). LC regeneration occurs in the testis of the EDS-treated rats from the differentiation of the precursor Leydig cells (PLC). This study was designed to investigate the patterns of change in the mRNAs for the luteinizing hormone receptor (LHR) and the steroidogenic enzymes, cholesterol side chain cleavage (P-450scc) and 17 alpha-hydroxylase (P-450(17 alpha)) during LC regeneration from PLCs. Mature (60 days of age) Sprague-Dawley male rats received a single intraperitoneal injection of EDS and were killed at different times between days 2 and 60 post-treatment. PLC- and LC-enriched fractions were isolated from the testes of the EDS-treated rats and age-matched control rats using a collagenase digestion-Percoll gradient method. Total RNA was extracted from these cell populations and subjected to Northern blot analysis. The LC fraction isolated from testes of control rats expressed four major transcripts of the LHR, sized 1.8, 2.5, 4.2 and 7.0 kb. The undifferentiated PLC fraction from controls expressed only a truncated form, the 1.8 kb transcript. This truncated LHR transcript was also the only LHR mRNA species detected in PLCs at day 2 post-EDS treatment. In contrast, all four transcripts of the LHR were detected in the PLC fraction at day 10 post-EDS treatment. The levels of the full length 7.0 kb transcript increased thereafter and reached a peak between days 24 and 36 post-EDS treatment in the PLC fraction. Concomitant with the increase in the 7.0 kb transcript, the truncated 1.8 kb transcript decreased in amount and reached a nadir between days 16 and 36 post-treatment. The changes observed in this cell fraction reflect the process of differentiation of PLCs into LCs. At day 45 post-EDS treatment, the level of the 7.0 kb transcript decreased while the 1.8 kb form increased in the PLC fraction, reflecting the completion of LC regeneration from this cell fraction. By day 60 post-EDS treatment, the levels of the 1.8 kb transcript rose to the value observed in undifferentiated control PLCs and the other transcripts were no longer detected in the PLC fraction, indicating that cells in the PLC fraction were again in an undifferentiated stage. Messenger RNAs for both the steroidogenic enzymes, P-450scc and P-450(17 alpha) were expressed in the control LC fraction. Neither of these two mRNAs were detected in the PLC fraction of the control rats. P-450scc and P-450(17 alpha) mRNAs were first expressed in the PLC fraction at day 10 post-EDS treatment. Thereafter, the levels of P-450scc and P-450(17 alpha) mRNAs increased in the PLC fraction and reached a peak between days 24 and 36 and days 24 and 45 post-EDS treatment respectively. P-450scc and P-450(17 alpha) mRNAs were no longer expressed in the PLC fraction at day 60 post-EDS treatment. These patterns also reflect the process of differentiation of PLCs into functional LCs. These results demonstrate for the first time that PLCs in the control testis are undifferentiated and do not express functional LHR and steroidogenic enzymes or their mRNAs. The PLCs are characterized, however, by the expression of a truncated 1.8 kb transcript of the LHR mRNA. Functional LHR and steroidogenic enzymes are expressed in PLCs only during their differentiation into LCs after EDS treatment. Subsequent to LC regeneration, the PLCs return to an undifferentiated stage.


2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Chang Ji ◽  
Wanling Xu ◽  
Zhiqing Zhang ◽  
Shuai Cui ◽  
Wei Yi

Polycystic ovarian syndrome (PCOS) is a common, complex, and heterogeneous endocrine and metabolic disorder. There is no standardized treatment, and it therefore requires individualized therapies according to the symptoms and pathogenesis of each patient. The present study aimed to determine the effect of electroacupuncture at the acupoints Zusanli (ST36), Sanyinjiao (SP6), and Neiguan (PC6) on reproductive disorders and insulin resistance in a murine model of PCOS induced by dehydroepiandrosterone (DHEA). Vaginal smear analysis was used to determine mice estrous cycle; intraperitoneal glucose and insulin tolerance tests were adopted to analyze metabolic characteristics; enzyme-linked immunosorbent assay was used to measure hormone levels; gene expression was quantified with real-time PCR; hematoxylin and eosin staining was used to observe ovarian morphology. We observed disordered estrous cycle, polycystic ovarian morphology, and higher levels of homeostasis model assessment-insulin resistance (HOMA-IR) and testosterone (T), indicating successful modeling of PCOS. DHEA increased levels of estrogen (E2), progesterone (P), testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH), and EA treatment restored them to levels seen in the control group. EA reduced the days in estrus caused by DHEA, improved the abnormal sex hormone receptor genes, and attenuated the DHEA-induced histomorphological changes in mouse ovaries. The average expressions of the androgen receptor (AR), estrogen receptor (ER), luteinizing hormone receptor (LHR), and follicle-stimulating hormone receptor (FSHR) genes in the ovary greatly increased after DHEA treatment and significantly decreased in the DHEA + EA group. After EA treatment, the cystic follicle (CF) number was reduced and corpora lutea (CL) increased in the DHEA + EA group compared to the DHEA group. EA improved glucose intolerance and insulin intolerance. Statistical analysis of intraperitoneal glucose tolerance test-area under curve (IPGTT-AUC) glucose levels revealed a significant decrease in DHEA group mice compared to the control and DHEA + EA groups. EA was found to restore fasting blood glucose, fasting serum insulin, and HOMA-IR. In summary, our study suggests that EA has a remarkable effect in the DHEA-induced murine PCOS model. Management of EA could improve estrous cycle, hormonal disorders, abnormal sex hormone receptors in ovaries, ovary morphology, and insulin resistance in PCOS mice.


2019 ◽  
Vol 20 (11) ◽  
pp. 2677
Author(s):  
Hiroshi Miyamoto

Sex steroids, including androgens, estrogens, and progestogens, are known to have widespread physiological actions beyond the reproductive system via binding to the sex hormone receptors, members of the nuclear receptor superfamily that function as ligand-inducible transcription factors [...]


Author(s):  
Thomas Buech ◽  
Pascal Nurwakagari ◽  
David Ben-Menahem ◽  
Thomas Gudermann

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