Lv Mengqing, Li Jiahui, Xing Ya, Zhou Xiaoyi, Ge Jing, Geng Tuoyu, Gong Daoqing, Zhao Minmeng
College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu Province 225009, PR China.
College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu Province 225009, PR China; Joint International Research Laboratory of Agriculture and Agri-Product Safety of Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu Province 225009, PR China.
Poult Sci. 2025 Jul 6;104(10):105515. doi: 10.1016/j.psj.2025.105515.
Protein Kinase A (PKA) is found in a wide range of body tissues and is involved in various cellular activities. PKA has been observed to interact with key proteins in the nuclear factor kappa-B (NF-κB) pathway to activate the pathway, thereby triggering an inflammatory response. However, the role of PKA in the anti-inflammatory mechanism of goose fatty liver remains to be elucidated. A total of 16 healthy 70-day-old male Lander geese were randomly divided into the control and overfeeding groups. Next, goose primary hepatocytes were treated with 200 mmol/L glucose. The protein levels of p-IκB, PKA and tumor necrosis factor alpha (TNFα) in the liver and hepatocytes, as well as the interaction of p-IκB and PKA were detected. Finally, the hepatocytes were treated with a combination of 200 mmol/L glucose and overexpressed or knocked-down PKA. The protein levels of p-IκB, PKA and TNFα were measured. The results showed that the levels of p-IκB, PKA and TNFα were significantly reduced (P < 0.05) in goose fatty liver compared to normal liver, and the interaction of p-IκB and PKA was inhibited in overfeeding group. The levels of p-IκB and PKA in 200 mmol/L glucose-treated hepatocytes were significantly reduced compared with control group (P < 0.05). Furthermore, the level of TNFα was unchanged (P > 0.05), and the interaction of p-IκB and PKA was inhibited in 200 mmol/L glucose-treated hepatocytes. The levels of p-IκB, PKA, and TNFα were significantly increased in the hepatocytes overexpressing PKA and treated with 200 mmol/L glucose compared to control group (P < 0.05). In contrast, the levels of p-IκB, PKA, and TNFα were significantly suppressed in the knockdown of PKA and treated with 200 mmol/L glucose compared with control group (P < 0.05). In conclusion, inflammation was suppressed in both the goose fatty liver and the hepatocytes treated with 200 mmol/L glucose. In addition, glucose inhibits inflammation in goose fatty liver by reducing the interaction between PKA and IκB.
蛋白激酶A(PKA)存在于多种身体组织中,并参与各种细胞活动。已观察到PKA与核因子κB(NF-κB)通路中的关键蛋白相互作用以激活该通路,从而引发炎症反应。然而,PKA在鹅脂肪肝抗炎机制中的作用仍有待阐明。将16只70日龄健康雄性朗德鹅随机分为对照组和过量饲喂组。接下来,用200 mmol/L葡萄糖处理鹅原代肝细胞。检测肝脏和肝细胞中p-IκB、PKA和肿瘤坏死因子α(TNFα)的蛋白水平,以及p-IκB与PKA的相互作用。最后,用200 mmol/L葡萄糖与过表达或敲低PKA的组合处理肝细胞。测量p-IκB、PKA和TNFα的蛋白水平。结果显示,与正常肝脏相比,鹅脂肪肝中p-IκB、PKA和TNFα的水平显著降低(P<0.05),且过量饲喂组中p-IκB与PKA的相互作用受到抑制。与对照组相比,200 mmol/L葡萄糖处理的肝细胞中p-IκB和PKA的水平显著降低(P<0.05)。此外,TNFα水平未发生变化(P>0.05),且200 mmol/L葡萄糖处理的肝细胞中p-IκB与PKA的相互作用受到抑制。与对照组相比,过表达PKA并用200 mmol/L葡萄糖处理的肝细胞中p-IκB、PKA和TNFα的水平显著升高(P<0.05)。相反,与对照组相比,敲低PKA并用200 mmol/L葡萄糖处理的肝细胞中p-IκB、PKA和TNFα的水平显著受到抑制(P<0.05)。总之,鹅脂肪肝和用200 mmol/L葡萄糖处理的肝细胞中的炎症均受到抑制。此外,葡萄糖通过减少PKA与IκB之间的相互作用来抑制鹅脂肪肝中的炎症。