College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China; College of Life Science, Xinyang Normal University, Xinyang 464000, China.
College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China.
Int Immunopharmacol. 2024 Jan 5;126:111153. doi: 10.1016/j.intimp.2023.111153. Epub 2023 Nov 17.
To investigate the regulatory effects of Chito-oligosaccharide (COS) on the anti-oxidative, anti-inflammatory, and MAPK signaling pathways. A total of 40 28-day-old weaned piglets were randomly allotted to 4 equal groups [including the control group, lipopolysaccharide (LPS) group, COS group, and COS*LPS group]. On the morning of d 14 and 21, piglets were injected with saline or LPS. At 2 h post-injection, whole blood samples were collected on d 14 and 21, and small intestine and liver samples were collected and analyzed on d 21. The results showed that COS inhibited the LPS-induced increase of malondialdehyde (MDA) concentration and hepatic TNF-α cytokines. COS significantly increased the serum total antioxidant capability (T-AOC) value on d 14, and total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) activities in both serum and liver on d 21. Furthermore, it increased hepatic catalase (CAT) activity. COS also increased the LPS-induced decrease in serum IgG concentrations. Immunohistochemical analysis results showed that COS significantly increased the jejunal and ileal Caspase 3, and ileal CD values challenged by LPS. Dietary COS decreased the LPS-induced jejunal and ileal BAX and CCL2 mRNA levels, markedly decreased ileal COX2 and SOD1 mRNA levels, while increasing ileal iNOS. Furthermore, COS significantly increased the LPS-induced jejunal and ileal p-P38 and MyD88, as well as jejunal P38, while it effectively suppressed jejunal JNK1, and jejunal and ileal JNK2, p-JNK1, and p-JNK2 protein expressions. These results demonstrated that COS could be beneficial by attenuating LPS-challenged intestinal inflammation via regulating mitochondrial apoptotic and MAPK signaling pathways.
为了研究壳寡糖（COS）对抗氧化、抗炎和 MAPK 信号通路的调节作用。将 40 头 28 日龄断奶仔猪随机分为 4 个相等的组[包括对照组、脂多糖（LPS）组、COS 组和 COS*LPS 组]。在第 14 天和 21 天的上午，仔猪分别注射生理盐水或 LPS。在注射后 2 小时，分别于第 14 天和第 21 天采集全血样本，第 21 天采集小肠和肝脏样本并进行分析。结果表明，COS 抑制了 LPS 诱导的丙二醛（MDA）浓度和肝 TNF-α 细胞因子的增加。COS 显著提高了第 14 天血清总抗氧化能力（T-AOC）值，以及第 21 天血清和肝脏中总超氧化物歧化酶（T-SOD）和谷胱甘肽过氧化物酶（GSH-PX）的活性。此外，它还增加了肝过氧化氢酶（CAT）的活性。COS 还增加了 LPS 诱导的血清 IgG 浓度降低。免疫组织化学分析结果表明，COS 显著增加了 LPS 诱导的空肠和回肠 Caspase 3 和回肠 CD 值。饲粮 COS 降低了 LPS 诱导的空肠和回肠 BAX 和 CCL2 mRNA 水平，显著降低了回肠 COX2 和 SOD1 mRNA 水平，同时增加了回肠 iNOS。此外，COS 显著增加了 LPS 诱导的空肠和回肠 p-P38 和 MyD88，以及空肠 P38，同时有效抑制了空肠 JNK1 以及空肠和回肠 JNK2、p-JNK1 和 p-JNK2 蛋白表达。这些结果表明，COS 通过调节线粒体凋亡和 MAPK 信号通路，可减轻 LPS 引起的肠道炎症。
