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Protective Effects of Syringic Acid Against Oxidative Damage, Apoptosis, Autophagy, Inflammation, Testicular Histopathologic Disorders, and Impaired Sperm Quality in the Testicular Tissue of Rats Induced by Mercuric Chloride
Environmental Toxicology ( IF 4.4 ) Pub Date : 2024-08-03 , DOI: 10.1002/tox.24395
Serkan Ali Akarsu 1 , Cihan Gür 2 , Sefa Küçükler 3 , Nurhan Akaras 4 , Mustafa İleritürk 5 , Fatih Mehmet Kandemir 6
Affiliation  

Mercury (Hg) is one of the most toxic heavy metals that damage testicular tissue. Mercury chloride (HgCl2) is one of the most toxic forms of mercury that can easily cross biological membranes. Syringic acid (SA) is a natural flavonoid found in many vegetables and fruits. In this study, the effects of SA against HgCl2‐induced testicular damage in rats were determined by biochemical, histopathological, and spermatological analyses. For this study, a total of 35 Spraque Dawley rats were used. Rats were divided into five groups as control, HgCl2, SA 50, HgCl2 + SA 25, and HgCl2 + SA 50. HgCl2 was administered intraperitoneal (IP) at a dose of 1.23 mg/kg/bw, while SA was administered by oral gavage at doses of 25 and 50 mg/kg/bw. The rats were then sacrificed, and testicular tissues were removed. HgCl2 caused an increase in MDA level and a decrease in SOD, CAT, and GPx activity and GSH level in the testicular tissue of rats. HgCl2 is involved in the increase of eIF2‐α, PERK, ATF‐4, ATF‐6, CHOP, NF‐κB, TNF‐α, IL‐1β, Apaf‐1, Bax, and Caspase‐3 mRNA expression. HgCl2 caused a decrease in sperm motility, an increase in the rate of abnormal sperm and sperm DNA fragmentation in rats. However, SA oral administration dose‐dependently inhibited endoplasmic reticulum stress, oxidative stress, inflammation, and apoptosis and preserved epididymal sperm quality and testicular histoarchitectures. In conclusion, SA had protective effects against HgCl2‐induced testicular oxidative damage, inflammation, endoplasmic reticulum stress, and apoptosis.

中文翻译:


丁香酸对氯化汞诱导的大鼠睾丸组织中氧化损伤、细胞凋亡、自噬、炎症、睾丸组织病理学疾病和精子质量受损的保护作用



汞 (Hg) 是损害睾丸组织的毒性最强的重金属之一。氯化汞 (HgCl2) 是毒性最强的汞形式之一,很容易穿过生物膜。丁香酸 (SA) 是一种天然类黄酮,存在于许多蔬菜和水果中。在本研究中,通过生化、组织病理学和精子学分析确定了 SA 对 HgCl2 诱导的大鼠睾丸损伤的影响。在本研究中,共使用了 35 只 Spraque Dawley 大鼠。将大鼠分为 5 组作为对照,分别为 HgCl2 、 SA 50 、 HgCl2 + SA 25 和 HgCl2 + SA 50 。HgCl2 以 1.23 mg/kg/bw 的剂量腹膜内 (IP) 给药,而 SA 以 25 和 50 mg/kg/bw 的剂量口服强饲法给药。然后处死大鼠,取出睾丸组织。HgCl2 导致大鼠睾丸组织中 MDA 水平升高,SOD 、 CAT 和 GPx 活性以及 GSH 水平降低。HgCl2 参与 eIF2-α、PERK、ATF-4、ATF-6、CHOP、NF-κB、TNF-α、IL-1β、Apaf-1、Bax 和 Caspase-3 mRNA 表达的增加。HgCl2 导致大鼠精子活力降低,异常精子和精子 DNA 片段化率增加。然而,SA 口服给药剂量依赖性地抑制内质网应激、氧化应激、炎症和细胞凋亡,并保留了附睾精子质量和睾丸组织结构。总之,SA 对 HgCl2 诱导的睾丸氧化损伤、炎症、内质网应激和细胞凋亡具有保护作用。
更新日期:2024-08-03
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