Sun Jianxu, Jiao Zitao, Zhu Weifeng, Li Xiuyu, Wang Panpan, Wang Jiangfeng, Tai Tiange, Wang Yuxi, Wang Haibin, Shi Guangliang
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Harbin, China.
Biol Trace Elem Res. 2023 May;201(5):2512-2523. doi: 10.1007/s12011-022-03327-y. Epub 2022 Jun 18.
Cadmium (Cd) can damage tissues by inducing oxidative stress, lymphocyte infiltration, and inflammation in these sites. Meanwhile, astilbin (Ast) is an antioxidant agent. At present, only a few mechanisms of Cd-induced adipose tissue damage have been described. Herein, we assessed the potential protective effects and the molecular mechanism underlying the antioxidant properly of Ast after Cd intake in chicken adipose tissue. In this study, a total of 160 7-day-old roosters were randomly divided into four groups. Roosters were fed with a basic diet (C group), Ast 40 mg/kg (Ast group), CdCl 150 mg/kg + Ast 40 mg/kg (Cd/Ast group), and CdCl 150 mg/kg (Cd group) for 60 days. We found that Cd intake changed the morphology and structure of adipose tissues and decreased the expression of several antioxidants, including total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and total antioxidant capacity (T-AOC), but increased those of oxidative stress markers including malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), NO, and H2O2. Cd further activated the nuclear factor kappa B (NF-κB) signaling pathway and increased the expression of the inflammation-related mediators, interleukin 1beta (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), cyclooxygenase-2 (COX-2), iNOS, prostaglandin E synthase (PTGES), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ). Cd-induced oxidative stress upregulated the expression of three heat shock proteins (HSPs), including HSP27, HSP70, and HSP90. Summarily, Cd causes oxidative stress-mediated tissue damage by activating the NF-κB pathway, promoting inflammation and upregulating the expression of HSPs. However, Ast supplementation modulates oxidative stress in adipose tissue by inhibiting inflammation mediated by the NF-κB pathway and regulating the expression of HSPs.
镉（Cd）可通过诱导氧化应激、淋巴细胞浸润以及这些部位的炎症来损害组织。同时，二氢杨梅素（Ast）是一种抗氧化剂。目前，关于镉诱导脂肪组织损伤的机制仅有少数被描述。在此，我们评估了二氢杨梅素在鸡摄入镉后对脂肪组织抗氧化作用的潜在保护效果及其分子机制。在本研究中，总共160只7日龄公鸡被随机分为四组。公鸡分别喂食基础日粮（C组）、40毫克/千克二氢杨梅素（Ast组）、150毫克/千克氯化镉 + 40毫克/千克二氢杨梅素（Cd/Ast组）以及150毫克/千克氯化镉（Cd组），持续60天。我们发现摄入镉改变了脂肪组织的形态和结构，并降低了几种抗氧化剂的表达，包括总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）和总抗氧化能力（T-AOC），但增加了氧化应激标志物的表达，包括丙二醛（MDA）、诱导型一氧化氮合酶（iNOS）、一氧化氮（NO）和过氧化氢（H2O2）。镉进一步激活了核因子κB（NF-κB）信号通路，并增加了炎症相关介质白细胞介素1β（IL-1β）、白细胞介素6（IL-6）、白细胞介素8（IL-8）、白细胞介素10（IL-10）、环氧化酶-2（COX-2）、iNOS、前列腺素E合酶（PTGES）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）的表达。镉诱导的氧化应激上调了三种热休克蛋白（HSPs）的表达，包括HSP27、HSP70和HSP90。总之，镉通过激活NF-κB途径、促进炎症反应和上调热休克蛋白的表达导致氧化应激介导的组织损伤。然而，补充二氢杨梅素可通过抑制NF-κB途径介导的炎症反应和调节热休克蛋白的表达来调节脂肪组织中的氧化应激。
