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山奈酚对百草枯诱发的大鼠睾丸毒性的治疗作用:一项基于生化和组织病理学的研究。

Curative effects of tectochrysin on paraquat-instigated testicular toxicity in rats: A biochemical and histopathological based study.

作者信息

Ijaz Muhammad Umar, Alvi Kaynat, Hamza Ali, Anwar Haseeb, Al-Ghanim Khalid A, Riaz Mian Nadeem

机构信息

Department of Zoology, Wildlife and Fisheries, University of Agriculture, Faisalabad, 38040, Pakistan.

Department of Physiology, Government College University of Faisalabad, Faisalabad, Pakistan.

出版信息

Heliyon. 2024 Feb 1;10(3):e25337. doi: 10.1016/j.heliyon.2024.e25337. eCollection 2024 Feb 15.

DOI:10.1016/j.heliyon.2024.e25337
PMID:38356568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10865255/
Abstract

BACKGROUND

Paraquat (PQ) is a herbicide that is used globally in the agriculture sector to eradicate unwanted weeds, however it also induces significant damages in various organs of the body such as testes. Tectochrysin (TEC) is an important flavonoid that shows versatile therapeutic potentials. Currently, there is no established antidote to cure PQ-induced testicular toxicity.

OBJECTIVE

The present study was conducted to evaluate the ameliorative effects of TEC against PQ prompted testicular damage.

METHODS

Sprague-Dawley rats (n = 48) were used to conduct the trial. Rats were allocated in to 4 groups i.e., Control, PQ administrated group (5 mgkg), PQ + TEC co-administrated group (5 mgkg + 2.5 mgkg) and TEC only administrated group (2.5 mgkg). The trial was conducted for 8 weeks. The activity of anti-oxidants and the levels of MDA and ROS were determined by spectrophotometric method. Steroidogenic enzymes as well as apoptotic markers expressions were evaluated by qRT-PCR. The level of hormones and inflammatory indices was quantified by enzyme-linked immunosorbent assay.

RESULTS

PQ exposure markedly (P < 0.05) disturbed the biochemical, spermatogenic and histological profile in the rats. Nevertheless, TEC treatment considerably (P < 0.05) increased CAT, GPx GSR and SOD activity, besides decreasing MDA and ROS contents. TEC administration also increased sperm viability, count and motility. 17β-HSD, 3β-HSD, StAR and Bcl-2 expressions were also increased following TEC administration. The supplementation of TEC substantially (P < 0.05) decreased Bax, Caspase-3 expression and the levels of inflammatory markers i.e., interleukin-1β (IL-1β), interleukin-6 (IL-6), nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) activity. Additionally, the levels of plasma testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were increased following TEC supplementation. Furthermore, TEC supplementation considerably decreased sperm structural abnormalities and histomorphological damages of the testes. The mitigative role of TEC might be due to its anti-inflammatory, anti-apoptotic, androgenic and anti-oxidant potentials.

CONCLUSION

Taken together, it is concluded that TEC can be used as a potential candidate to treat testicular toxicity.

摘要

背景

百草枯(PQ)是一种除草剂,在全球农业领域用于根除杂草,但它也会对身体的各个器官如睾丸造成严重损害。tectochrysin(TEC)是一种重要的黄酮类化合物,具有多种治疗潜力。目前,尚无已确立的解药来治疗PQ诱导的睾丸毒性。

目的

本研究旨在评估TEC对PQ引起的睾丸损伤的改善作用。

方法

使用Sprague-Dawley大鼠(n = 48)进行试验。将大鼠分为4组,即对照组、PQ给药组(5 mg/kg)、PQ + TEC联合给药组(5 mg/kg + 2.5 mg/kg)和仅TEC给药组(2.5 mg/kg)。试验持续8周。通过分光光度法测定抗氧化剂活性以及丙二醛(MDA)和活性氧(ROS)水平。通过定量逆转录聚合酶链反应(qRT-PCR)评估类固醇生成酶以及凋亡标志物的表达。通过酶联免疫吸附测定法定量激素水平和炎症指标。

结果

PQ暴露显著(P < 0.05)扰乱了大鼠的生化、生精和组织学特征。然而,TEC治疗显著(P < 0.05)提高了过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GSR)和超氧化物歧化酶(SOD)的活性,同时降低了MDA和ROS含量。给予TEC还提高了精子活力、数量和运动能力。给予TEC后,17β-羟基类固醇脱氢酶(17β-HSD)、3β-羟基类固醇脱氢酶(3β-HSD)、类固醇急性调节蛋白(StAR)和Bcl-2的表达也增加。补充TEC显著(P < 0.05)降低了Bax、半胱天冬酶-3(Caspase-3)的表达以及炎症标志物即白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、核因子κB(NF-κB)、肿瘤坏死因子-α(TNF-α)和环氧合酶-2(COX-2)的活性。此外,补充TEC后血浆睾酮、促卵泡生成素(FSH)和促黄体生成素(LH)水平升高。此外,补充TEC显著降低了精子结构异常和睾丸的组织形态学损伤。TEC的减轻作用可能归因于其抗炎、抗凋亡、雄激素生成和抗氧化潜力。

结论

综上所述,得出结论:TEC可作为治疗睾丸毒性的潜在候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/cef7385dd82b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/f80deb38d2e9/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/0f8ec10de271/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/cef7385dd82b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/f80deb38d2e9/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/0f8ec10de271/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a754/10865255/cef7385dd82b/gr3.jpg

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