Objective 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 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 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, 3 β -hydroxysteroid dehydrogenase 1 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 DS Jinghuosu protects against TG-induced reproductive system injury in rats, probably by improving zinc homeostasis, enhancing the testosterone synthesis and attenuating oxidative stress.

The long-term use of tripterygium glycosides (TG) can lead to male reproductive damage. Research indicates that zinc and selenium exhibit a synergistic effect in the male reproductive system, with the combined preparation demonstrating superior therapeutic effects compared to individual preparations. The purpose of this study was to explore the specific mechanism by which zinc and selenium mitigate reproductive toxicity induced by TG in male rats. Rats were randomly assigned to three groups: control group (C group), model group (M group, receiving TG at 30 mg/kg/day), and model + zinc + selenium group (ZS group). The ZS group was also given TG gavage for the first 4 weeks. Starting from the fifth week until the conclusion of the eighth week, the ZS group received an additional protective treatment of 10 mg/kg/day Zn and 0.1 mg/kg/day Se 4 h after TG administration. Following euthanasia, blood samples, rat testis, and epididymis tissues were collected for further experiments. Combined zinc-selenium treatment corrects the imbalance of zinc-selenium homeostasis in testicular tissue induced by TG. This is achieved by upregulating the expression of metal transcription factor (MTF1) and zinc transporters ZIP8 and ZIP14 and downregulating the expression of ZnT10. Improvement of zinc and selenium homeostasis enhanced the expression of zinc-containing enzymes (ADH, LDH, and ALP) and selenoproteins (GPx1 and SELENOP) in the testis. At the same time, zinc and selenium mitigate TG-induced reproductive damage by promoting the activity of antioxidant enzymes and upregulating the expression of proteins associated with the oxidative stress pathway, including Nrf2, Keap1, HO-1, PI3K, and p-AKT.

Background: Zinc (Zn)is an essential trace element for spermatogenesis and its deficiency causes abnormal spermatogenesis. Objective: The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs sperm morphology and its reversibility. Methods: 30 SPF grade male Kunming (KM) mice were randomly divided into three groups, 10 mice per group. Zn-normal diet group (ZN group) was given Zn-normal diet(Zn content= 30 mg/kg)for 8 weeks. Zn-deficienct diet group (ZD group) was given Zn-deficienct diet(Zn content< 1 mg/kg)for 8 weeks. Zn-deficient and Znnormal diet group(ZDN group)was given 4 weeks Zn-deficienct diet followed by 4 weeks Zn-normal diet. After 8 weeks, the overnight fasted mice were sacrificed, and blood and organs were collected for further analysis. Results: The experimental results showed that Zn-deficienct diet leads to increased abnormal morphology sperm and testicular oxidative stress.The rate of abnormal morphology sperm, chromomycin A3(CMA3), DNA fragmentation index (DFI), malondialdehyde (MDA) were significantly increased, and a-kinase anchor protein 4 (AKAP4), dynein axonemal heavy chain 1(DNAH1), sperm associated antigen 6(SPAG6), cilia and flagella associated protein 44(CFAP44), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), nuclear factor erythroid 2-related factor (NRF2), NAD(P)H:quinone oxidoreductase 1(NQO1) and heme oxygenase 1(HO1) were significantly decreased in the ZD group mice. While the changes in above indicators caused by Zn-deficient diet were significantly alleviated in the ZDN group. Conclusion: It was concluded that Zn-deficient diet causes abnormal morphology sperm and testicular oxidative stress in male mice. Abnormal morphology sperm caused by Zn-deficient diet are reversible, and Zn-normal diet can alleviate them.

不孕不育症是一个亟待解决的全球性公共卫生问题,影响着全球10％～15％的育龄夫妇,其中男性因素占50％[1-2].男性不育病因复杂,往往受多重因素的影响.其中遗传因素是研究的热点之一,一般认为参与精子发生的相关基因突变导致精子发生障碍进而造成 男性不育[3].

目的 鉴定高尿酸血症模型大鼠睾丸组织中差异表达的长链非编码RNA(lncRNA).方法 苏木素伊红(HE)染色法观察大鼠睾丸组织病理形态,从对照组和高尿酸血症组雄性SD大鼠睾丸组织中分别提取RNA进行测序,筛选出两组间差异表达的lncRNA,对其进行靶基因预测,并将lncRNA和mRNA进行GO和KEGG功能富集分析.结果 高尿酸血症组睾丸组织结构受损.与对照组相比,筛选获得差异表达的lncRNA有89个(上调42个、下调47个);差异表达mRNA有50个(上调29个、下调21个).GO富集分析结果显示,这些差异表达lncRNA主要与胰岛素受体信号通路的调节、炎症反应的调节、发育过程及G-蛋白偶联谷氨酸受体结合相关.KEGG通路富集分析结果显示,差异表达lncRNA主要富集在胰岛素信号通路、cGMP-PKG信号通路、cAMP信号通路及钙信号通路上.结论 高尿酸血症大鼠睾丸组织中lncRNA的表达有差异,有助于阐明lncRNA在高尿酸血症导致雄性大鼠生殖障碍的潜在作用.

Zinc (Zn) is an essential trace element for human growth and its deficiency causes huge health impacts. The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs reproductive function and its reversibility. Hence, SPF grade male Kunming (KM) mice were divided into three groups. Zn-normal diet group (ZN group) was provided with Zn-normal diet (Zn content = 30 mg/kg, DY19410Y) for 8 weeks. Zn-deficient diet group (ZD group) was provided with Zn-deficient diet (Zn content < 1 mg/kg, DY19401) for 8 weeks. Zn-deficient and Zn-normal diet group (ZDN group) was provided with 4 weeks Zn-deficient diet followed by 4 weeks Zn-normal diet. After 8 weeks, the overnight-fasted mice were sacrificed, and blood and organs were collected for further analysis. The results showed that Zn-deficient diet caused testicular structural disorders, decreased semen quality, imbalance in zinc homeostasis, and impaired autophagy. Semen quality, testosterone, serum Zn, testicular tissue Zn, testicular free Zn ions, alkaline phosphatase (ALP), zinc transporter 7(ZnT7), Beclin1, autophagy-related 5(ATG5), and the ratio of light chain 3(LC3) II/LC3I were significantly decreased, and ZnT4, Zrt-, Irt-like protein7 (ZIP7), and ZIP13 expression were significantly increased in ZD group mice, while the changes in above indicators caused by Zn-deficient diet were significantly alleviated in the ZDN group. It was concluded that Zn-deficient diet causes testicular structural disorders and decreased semen quality by causing imbalances in Zn homeostasis and impaired autophagy in male mice. Reproductive damages caused by Zn-deficient diet are reversible, and Zn-normal diet can alleviate them.

Three new Pb(II) coordination polymers, namely [Pb-2(mand)(2)](n) (1), {[Pb(L-Hmand)(NO3)(5,5'-DM-2,2'-bipy)]center dot 2H(2)O}(n) (2-L), {[Pb(D-Hmand)(NO3)(5,5'-DM-2,2'-bipy)]center dot 2H(2)O} n (2-D) (H(2)mand = D/L-mandelic acid, 5,5'-DM-2,2'-bipy = 5,5'-dimethyl-2,2'-bipyridyl), have been prepared. Their structures have been determined by single-crystal X-ray diffraction analyses and further characterized by elemental analyses, powder X-ray diffraction and thermogravimetric analyses. Complex 1 crystallizes in the triclinic system with space group P-1, and displays a 2D layer structure. Complexes 2-L and 2-D are pairs of enantiomers. They crystallize in the same chiral space group P2(1)2(1)2(1) and feature a 1D chain structure. The influence of the temperature and steric-hinerance of 5,5'-dimethyl-2,2'-dipyridyl molecules on constructing enantiomeric Pb(H) coordination polymers based on chiral mandelic acid ligands have been demonstrated. In addition, the circular dichroism (CD) spectroscopy of 2-L and 2-D exhibit obvious positive or negative Cotton effects indicating their homochirality. The luminescent properties of 1, 2-L and 2-D in the solid state have also been investigated.