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来源于人参茎叶的皂苷通过抑制 MAPK 介导的氧化应激和细胞凋亡来减轻阴囊热诱导的雄性生殖损伤。

Saponins derived from the stems and leaves of Panax ginseng attenuate scrotal heat-induced spermatogenic damage via inhibiting the MAPK mediated oxidative stress and apoptosis in mice.

机构信息

College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China.

Intelligent Synthetic Biology Center, Daejeon, Republic of Korea.

出版信息

Phytother Res. 2021 Jan;35(1):311-323. doi: 10.1002/ptr.6801. Epub 2020 Aug 6.

Abstract

Heat stress (HS) reaction is a stress response caused by adverse conditions. Currently, the incidence of reproductive malignancies particularly in males has been constantly increasing. This work investigated the effects of saponins derived from the stems and leaves of Panax ginseng (GSLS) on testicular injury induced by scrotal hyperthermia in mice. GSLS (150, 300 mg/kg) were administered intragastrically to mice for 14 days, then exposed to a single scrotal heat treatment at 43°C for 18 min on seventh day. HS induced a significant loss of multinucleate giant cells, desquamation of germ cells in destructive seminiferous tubules. Moreover, HS reduced the serum testosterone, testicular tissue superoxide dismutase activity and glutathione (GSH) content, while significantly enhanced the production of malondialdehyde (p < .05). GSLS exhibited the protective potential against HS-induced injury not only by modulating Bcl-2 family and caspase protease family, but also by suppressing the protein levels of heme oxygenase-1 (HO-1), heat shock protein 70 (HSP70), hypoxia inducible factor-1α (HIF-1α) and activation of Mitogen-activated protein kinase (MAPK) signaling pathways (p < .05). In conclusion, we clearly demonstrated that GSLS exhibited a significant protective effect against HS-induced testicular dysfunction, mainly the inhibition of oxidative stress associated apoptosis partly via regulation of the MAPK signaling pathway.

摘要

热应激(HS)反应是由不利条件引起的应激反应。目前,生殖系统恶性肿瘤的发病率,尤其是男性,一直在不断上升。本研究探讨了从人参茎叶中提取的皂苷(GSLS)对阴囊高温引起的雄性小鼠睾丸损伤的影响。GSLS(150、300mg/kg)灌胃给药,连续 14 天,第 7 天单次阴囊热暴露于 43°C 18 分钟。HS 导致多形核巨细胞大量丢失,破坏的生精小管中生殖细胞脱落。此外,HS 降低了血清睾酮、睾丸组织超氧化物歧化酶活性和谷胱甘肽(GSH)含量,同时显著增加了丙二醛(MDA)的产生(p<0.05)。GSLS 通过调节 Bcl-2 家族和半胱天冬酶蛋白酶家族,不仅表现出对 HS 诱导损伤的保护潜力,还通过抑制血红素加氧酶-1(HO-1)、热休克蛋白 70(HSP70)、缺氧诱导因子-1α(HIF-1α)的蛋白水平和丝裂原活化蛋白激酶(MAPK)信号通路的激活(p<0.05)。总之,我们明确表明,GSLS 对 HS 引起的睾丸功能障碍具有显著的保护作用,主要是通过抑制与氧化应激相关的细胞凋亡来发挥作用,部分机制与调节 MAPK 信号通路有关。

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