Liu Yongping, Mao Xiaojiang, Song Kai, Wang Ling, Li Xueshan, Zhang Chunxiao, Lu Kangle, Rahimnejad Samad
State Key Laboratory for Mariculture Breeding, Fisheries College, Jimei University, Xiamen, 361021, China.
State Key Laboratory for Mariculture Breeding, Fisheries College, Jimei University, Xiamen, 361021, China.
Fish Shellfish Immunol. 2025 Aug;163:110423. doi: 10.1016/j.fsi.2025.110423. Epub 2025 May 15.
An 8-week feeding experiment was carries out to explore the impacts of dietary tauroursodeoxycholic acid (TUDCA) on growth and gut integrity in spotted seabass (Lateolabrax maculatus) under heat stress (33 °C). Three hundred fish (2 ± 0.02 g) were allocated to triplicate groups and fed five diets containing graded levels of TUDCA at 0, 10, 20, 30, or 40 mg/kg (designated as Con, T10, T20, T30 and T40 diets). Growth performance was significantly (P < 0.05) enhanced in fish receiving ≥30 mg/kg TUDCA compared to the control group. Progressive increases in intestinal total antioxidant capacity and superoxide dismutase activity, accompanied by decreased malondialdehyde concentration, were observed as TUDCA dose increased. TUDCA application modulated the expression of intestinal antioxidant-related genes, downregulating keap1 and upregulating nrf2. Notably, supplementation with 40 mg/kg TUDCA improved intestinal morphology, as evidenced by increased villus height and number. Furthermore, in the T40 group, a marked downregulation of pro-apoptotic genes (caspase3, caspase8, caspase9, and bax) and reduced immunofluorescence intensity were observed, while the expression of the anti-apoptotic gene bcl was significantly up-regulated. Additionally, the expression of pro-inflammatory genes (il-1β, il-8, and tnf-α) and immunofluorescence intensity were significantly reduced in the T40 group compared to control. In contrast, the expression of anti-inflammatory genes (il-4, il-10, and tgf-β) was markedly upregulated. Furthermore, dietary inclusion of 40 mg/kg TUDCA suppressed the expression of endoplasmic reticulum stress-related genes (grp78, chop, perk, atf6, and ire1) and activated the bile acid receptor gene tgr5 in the intestine. Concurrently, TUDCA treatment enhanced the PI3K-Akt signaling pathway, contributing to the inhibition of apoptosis. The data generated in this study demonstrated that dietary supplementation with 40 mg/kg TUDCA promotes growth, activates the Nrf2-Keap1 and PI3K-AKT signaling pathways, enhances intestinal antioxidant defenses, suppresses inflammation and apoptosis, alleviates endoplasmic reticulum stress, and mitigates the physiological impacts of heat stress in L. maculatus reared at elevated temperatures.
进行了一项为期8周的饲养实验,以探究在热应激(33°C)条件下,饲料中牛磺熊去氧胆酸(TUDCA)对斑尾鲈(Lateolabrax maculatus)生长和肠道完整性的影响。将300尾鱼(2±0.02克)分为三组,每组重复,投喂五种含有不同水平TUDCA的饲料,其含量分别为0、10、20、30或40毫克/千克(分别称为对照组、T10、T20、T30和T40组饲料)。与对照组相比,摄入≥30毫克/千克TUDCA的鱼的生长性能显著提高(P<0.05)。随着TUDCA剂量的增加,肠道总抗氧化能力和超氧化物歧化酶活性逐渐增加,同时丙二醛浓度降低。TUDCA的应用调节了肠道抗氧化相关基因的表达,下调了keap1并上调了nrf2。值得注意的是,补充40毫克/千克TUDCA改善了肠道形态,绒毛高度和数量增加证明了这一点。此外,在T40组中,观察到促凋亡基因(caspase3、caspase8、caspase9和bax)明显下调,免疫荧光强度降低,而抗凋亡基因bcl的表达显著上调。此外,与对照组相比,T40组中促炎基因(il-1β、il-8和tnf-α)的表达和免疫荧光强度显著降低。相反,抗炎基因(il-4、il-10和tgf-β)的表达明显上调。此外,饲料中添加40毫克/千克TUDCA可抑制内质网应激相关基因(grp78、chop、perk、atf6和ire1)的表达,并激活肠道中的胆汁酸受体基因tgr5。同时,TUDCA处理增强了PI3K-Akt信号通路,有助于抑制细胞凋亡。本研究得出的数据表明,饲料中补充40毫克/千克TUDCA可促进生长,激活Nrf2-Keap1和PI3K-AKT信号通路,增强肠道抗氧化防御,抑制炎症和细胞凋亡,减轻内质网应激,并减轻高温饲养的斑尾鲈热应激的生理影响。