A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides
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Original Article|Updated:2024-03-22
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A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides
A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides
中国结合医学杂志(英文版)2024年30卷第4期 页码:330-338
Affiliations:
1.Hebei Key Laboratory of Reproductive Medicine, Hebei Institute of Reproductive Health, Hebei Reproductive Health Hospital, Shijiazhuang (050071), China
2.Graduate School of Hebei Medical University, Shijiazhuang (050017), China
3.School of Chemistry and Materials Science, Hebei Normal University, Shijiazhuang (050024), China
4.Xingtai Infertility Specialist Hospital, Xingtai, Hebei Province (054000), China
Author bio:
Prof. WANG Shu-song, E-mail: wshsong@126.com
Funds:
S&T Program of Hebei Province(226Z7722G);Government Clinical Medical Talent Training Program(ZF2023175)
A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides[J]. 中国结合医学杂志(英文版), 2024,30(4):330-338.
MA Jing, SUN Bo, TE Li-ger, et al. A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides[J]. Chinese Journal of Integrative Medicine, 2024,30(4):330-338.
A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides[J]. 中国结合医学杂志(英文版), 2024,30(4):330-338. DOI: 10.1007/s11655-023-3750-9.
MA Jing, SUN Bo, TE Li-ger, et al. A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides[J]. Chinese Journal of Integrative Medicine, 2024,30(4):330-338. DOI: 10.1007/s11655-023-3750-9.
A Dietary Supplement Jinghuosu Ameliorates Reproductive Damage Induced by Tripterygium Glycosides
摘要
Abstract
Objective:
2
To determine the possible protective effects of Jinghuosu
a dietary supplement (DS)
on tripterygium glycosides (TG)-induced reproductive system injury in rats and its underlying mechanisms.
Methods:
2
A reproductive damage model was established in rats by feeding of TGs. Twenty-eight male Sprague Dawley rats were randomly divided into 4 groups using a random number table (
n
=7 in each): control (C) group
model (M) group
DS group and L-carnitine (LC) group. Rats in M
DS and LC groups received 40 mg/kg TGs orally. Starting from the 5th week
after administration of TGs for 4 h every day
rats in DS and LC groups were administered with 2.7 g/kg DS and 0.21 g/kg LC
respectively
for protective treatment over the next 4 weeks. Rats in Group C continued to receive the control treatment. Hematoxylin-eosin staining was used for histopathological analysis of rat testicular tissues. Enzyme-linked immunosorbent assay was performed to measure alkaline phosphatase (ALP)
lactate dehydrogenase
alcohol dehydrogenase
total antioxidant capacity (T-AOC)
superoxide dismutase
glutathione peroxidase (GSH-Px)
and malondialdehyde (MDA) concentrations. Chemiluminescence assay was used to determine the serum testosterone content. Quantitative real-time PCR and Western blotting were conducted to analyze the expression of genes and proteins related to the testosterone synthesis pathway and the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 antioxidant pathway.
Results:
2
Oral administration of TGs induced significant increases in the testicular levels of zinc transporter 1 and MDA (
P
<
0.05). On the other hand
sperm concentration
sperm motility
and serum testosterone
serum zinc
testicular zinc
Zrt-
Irt-like protein 1
ALP
luteinizing hormone (LH) receptor
steroidogenic acute regulatory protein
Cytochrome P450 family 11 subfamily A member 1
3β-hydroxysteroid dehydrogenase1
T-AOC
GSH-Px
nuclear factor erythroid 2-related factor 2
heme oxygenase-1 and NAD (P)H: quinone oxidoreductase 1 levels decreased following TGs exposure (
P
<
0.05). All of these phenotypes were evidently reversed by DS (
P
<
0.05).
Conclusion:
2
DS Jinghuosu protects against TG-induced reproductive system injury in rats
probably by improving zinc homeostasis
enhancing the testosterone synthesis and attenuating oxidative stress.
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