Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education in Ningxia Medical University, Yinchuan, China.
Institute of Human Stem Cell Research, The General Hospital of Ningxia Medical University, Yinchuan, China.
Pharm Biol. 2021 Dec;59(1):1314-1325. doi: 10.1080/13880209.2021.1961822.
L. (Solanaceae) seed oil (LBSO) exerts LBSO exerts protective effects in the testis and via upregulating SIRT3.
This study evaluates the effects and mechanism of LBSO in the d-galactose (d-gal)-induced ageing testis.
Male Sprague Dawley (SD) rats ( = 30, 8-week-old) were randomly divided into three groups: LBSO group ( = 10) where rats received subcutaneous injection of d-gal at 125 mg/kg/day for 8 weeks and intragastric administration of LBSO at 1000 mg/kg/day for 4 weeks, ageing model group ( = 10) received 8-week-sunbcutaneous injection of d-gal, and control group ( = 10) with same administration of normal saline. Lentivirus had established TM4 cells with SIRT3 overexpression or silencing before LBSO intervened .
Treatment with LBSO, the levels of INHB and testosterone both increased, compared to ageing model. , we found the ED of LBSO was 86.72 ± 1.49 and when the concentration of LBSO at 100 μg/mL to intervene TM4 cells, the number of cells increased from 8120 ± 676.2 to 15251 ± 1119, and the expression of SIRT3, HO-1, and SOD upregulated. However, HO-1 and SOD were dysregulated by silencing SIRT3. On the other hand, the expression of AMPK and PGC-1 upregulated as an effect of SIRT3 overexpression by lentivirus, meanwhile the same increasing trend of that being found in cells treated with LBSO, compared to control group.
LBSO alleviated oxidative stress in d-gal-induced sub-acutely ageing testis and TM4 cells by suppressing the oxidative stress to mitochondria via SIRT3/AMPK/PGC-1α.
龙舌兰（Solanaceae）籽油（LBSO）通过上调 SIRT3 在睾丸中发挥保护作用。
本研究评估 LBSO 在半乳糖（d-gal）诱导的衰老睾丸中的作用和机制。
雄性 Sprague Dawley（SD）大鼠（n=30，8 周龄）随机分为三组：LBSO 组（n=10），大鼠接受皮下注射 d-gal 125mg/kg/天 8 周，并每天灌胃 LBSO 1000mg/kg/天 4 周；衰老模型组（n=10）接受 8 周皮下注射 d-gal；对照组（n=10）给予相同剂量的生理盐水。LBSO 干预前，慢病毒建立了 SIRT3 过表达或沉默的 TM4 细胞。
与衰老模型组相比，LBSO 治疗后 INHB 和睾酮水平均升高。我们发现 LBSO 的 ED 为 86.72±1.49，当 LBSO 浓度为 100μg/mL 干预 TM4 细胞时，细胞数量从 8120±676.2 增加到 15251±1119，SIRT3、HO-1 和 SOD 的表达上调。然而，沉默 SIRT3 会导致 HO-1 和 SOD 失调。另一方面，通过慢病毒过表达 SIRT3，AMPK 和 PGC-1 的表达上调，同时与对照组相比，LBSO 处理的细胞也出现了相同的上调趋势。
LBSO 通过 SIRT3/AMPK/PGC-1α 抑制氧化应激对线粒体的影响，缓解 d-gal 诱导的亚急性衰老睾丸和 TM4 细胞中的氧化应激。
