Pectinase-treated Panax ginseng ameliorates hydrogen peroxide-induced oxidative stress in GC-2 sperm cells and modulates testicular gene expression in aged rats

Kopalli, Spandana Rajendra; Cha, Kyu-Min; Jeong, Manbok; Lee, Sang-Ho; Sung, Jong-Hwan; Seo, Seok Kyo; Kim, Si-Kwan

doi:10.1016/j.jgr.2015.08.005

Cited by 35 publications

(33 citation statements)

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“…Many sex hormones such as FSH, LH and androgens are vital in the process of germ cell apoptosis and survival (Xu et al 2016). However, as described in our previous studies, GINST treatment attenuated the declining levels of sex hormones (Won et al 2014, Kopalli et al 2016 and the sex hormone receptors. In agreement with these findings, heat stress lowered the levels of sex hormone receptors, and consequently, increased germ cell apoptosis.…”

Section: Figuresupporting

confidence: 55%

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

Kim

Cha²,

Hwang³

et al. 2017

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Testicular hyperthermia is well studied to cause impaired spermatogenesis. In the present study, the protective effect of enzymatically modified (pectinase-treated) (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 ( < 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 ( < 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 factors and has considerable potential to be developed as a useful supplement in improving male fertility.

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Section: Figuresupporting

confidence: 55%

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

Kim

Cha²,

Hwang³

et al. 2017

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“…Hydrogen peroxide (H 2 O 2 ) (Fisher Scientific, Leicestershire, UK) was used as a positive control to assess the effect of the CJ extracts on cell viability after oxidative stress. 30 The cells were pretreated with CJ extracts at the indicated concentrations (0.001%, 0.01%, and 0.1%) for 1 hour before exposure to H 2 O 2 (200 lM). Exposure to H 2 O 2 lasted for 30 minutes.…”

Section: Culture Of Hce Cells and Cell Viability Assaymentioning

confidence: 99%

Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Lee

Choi

Cui

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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Citation: Lee HS, Choi J-H, Cui L, et al. Anti-inflammatory and antioxidative effects of Camellia japonica on human corneal epithelial cells and experimental dry eye: in vivo and in vitro study. Invest Ophthalmol Vis Sci. 2017;58:119658: -120758: . DOI:10.1167 PURPOSE. To analyze the anti-inflammatory and antioxidative effects of Camellia japonica (CJ) on human corneal epithelial (HCE) cells and its therapeutic effects in a mouse model of experimental dry eye (EDE). METHODS.Camellia japonica extracts of varying concentrations (0.001%, 0.01%, and 0.1%) were used to treat HCE cells. Dichlorofluorescein diacetate (DCF-DA) and dihydroethidium (DHE) assays were performed. The production of peroxiredoxin (PRX) 1-6 and manganesedependent superoxide dismutase (MnSOD) in HCE cells was assessed using Western blot analysis. Furthermore, eye drops containing 0.001%, 0.01%, or 0.1% CJ extract or a balanced salt solution (BSS) were applied to the EDE. Clinical parameters were measured 7 days after treatment. The levels of inflammatory markers and intracellular reactive oxygen species (ROS) were measured.RESULTS. Treatment with 0.01% and 0.1% CJ extracts decreased apoptosis in HCE cells. In addition, band intensities of PRX 1, 4, and 5, as well as MnSOD, after hydrogen peroxide (H 2 O 2 ) treatment showed a significant improvement after pretreatment with 0.01% and 0.1% CJ extracts. Mice treated with 0.1% CJ extract showed significantly improved clinical parameters when compared to those of the EDE control and BSS groups. A significant decrease in the levels of inflammatory markers and intracellular ROS was observed in the 0.01% and 0.1% CJ extract groups.CONCLUSIONS. Camellia japonica extracts promoted antioxidative protein expression and suppressed apoptosis in HCE cells. Furthermore, CJ extracts improved clinical signs of dry eye and reduced oxidative stress and the expression of inflammatory markers, suggesting that eye drops containing CJ extract could be used as an adjunctive treatment for dry eye.

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“…Mouse pachytene spermatocyte-derived cell line GC-2 were obtained from Zhong Yuan biological Ltd (Beijing, China) and were cultured in DMEM as described previously (Kopalli et al 2016). Where indicated, hypoxia (1% O 2 ) was achieved by a mixture of ultra-high purity gases (5% CO 2 , 10% H 2 and 85% N 2 ) in a 37°C hypoxia workstation (Invivo 2 , Baker Ruskinn, Sanford, ME, USA).…”

Section: Introductionmentioning

confidence: 99%

Elevation of autophagy rescues spermatogenesis by inhibiting apoptosis of mouse spermatocytes

Yin

Yang

et al. 2018

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Autophagy and apoptosis are interlocked in an extensive crosstalk. Our previous study demonstrated that hypotonic hypoxia-induced marked apoptosis of a spermatocyte-derived cell line (GC-2). However, whether hypoxia-induced apoptosis is mediated by inhibition of autophagy under hypoxic conditions remains unclear. In this study, GC-2 cells were cultured in 1% O 2 and harvested at different time points. Autophagy was determined by acridine orange staining, cyto-ID staining, mCherry-GFP-LC3B adenovirus transfection and Western blotting for various autophagy markers. Apoptosis was detected by TUNEL staining, flow cytometry, JC-1 staining and Western blotting of apoptosis-related proteins. We found that hypoxia-induced apoptosis of GC-2 cells through mitochondrial and death receptor pathways and inhibited autophagic flux in GC-2 cells in a time-dependent manner. However, while marked autolysosome formation was observed in GC-2 cells before 24-h culture in hypoxic conditions, apparent apoptosis was observed only after 24-h culture in hypoxic conditions. Caspase-8 siRNA treatment induced cell survival, accompanied by induction of the mature autophagosome, acidic vesicular organelle formation and autophagic flux. Furthermore, Beclin-1 overexpression markedly attenuated the impairment of spermatogenesis in mice by inhibiting apoptosis of spermatocytes. The results of this study demonstrate that hypoxia inhibits autophagy, which further enhances hypoxia-induced apoptosis of mouse spermatocytes by promoting caspase-8 activation in a time-dependent manner, suggesting that combined application of apoptosis inhibition and autophagy activation might be a therapeutic strategy for treating hypoxia-induced male infertility.Reproduction (2018) 156 545-558 546 Reproduction (2018) 156 545-558 https://rep.bioscientifica.com The activation of apoptosis can also inhibit autophagy under hypoxia. Caspases that are activated during apoptosis, mainly caspase-8 and caspase-3, can cleave autophagy-related proteins, such as ATG3, ATG4D and Beclin1, suppressing autophagy and resulting in cell damage (Li et al. 2011, Oral et al. 2012, Lamy et al. 2013). In addition, autophagy can block the induction of apoptosis and attenuate cellular injury under hypoxia. The activation of autophagy inhibits apoptosis by clearing damaged mitochondria, inhibiting caspase-3 activation and clearing reactive oxygen species (ROS)-damaged proteins. Thus, autophagy plays a protective role under hypoxia (Zhang et al. 2013, Li et al. 2014). However, in specific cases, autophagy or autophagy-relevant proteins may help in inducing apoptosis, which can aggravate cellular injury under hypoxia. The underlying mechanisms include the activation of caspases and clearance of the Bruce protein (an anti-apoptotic protein, a member of the inhibitors of apoptosis proteins family) (Nezis et al. , Young et al. 2012. Taking all the above into consideration, the interaction between autophagy and apoptosis in spermatocytes under hypoxia treatment remains unclear.In our previous study, we...

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Pectinase-treated Panax ginseng ameliorates hydrogen peroxide-induced oxidative stress in GC-2 sperm cells and modulates testicular gene expression in aged rats

Cited by 35 publications

References 49 publications

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

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

Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Elevation of autophagy rescues spermatogenesis by inhibiting apoptosis of mouse spermatocytes

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