Department of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, P.R. China.
Department of Thyroid and Breast Surgery, Suzhou Wuzhong People's Hospital, Suzhou, P.R. China.
In Vivo. 2023 Jul-Aug;37(4):1609-1618. doi: 10.21873/invivo.13246.
BACKGROUND/AIM: Acute liver injury is the hallmark of organ failure in sepsis. Enteral nutrition (EN) is an important clinical therapeutic measure in septic patients. However, the therapeutic effect of EN alone is not obvious. Here, we investigated whether octanoic acid (OA)-rich EN alleviated acute liver injury through PPARγ/STAT-1/MyD88 pathway in endotoxemic rats.
First, rats were randomly divided into four groups: Sham, Lipopolysaccharide (LPS), LPS+EN and LPS+EN+OA groups to investigate the effect of OA-rich EN on LPS-induced acute liver injury in endotoxemic rats. Then rats were randomly divided into five groups: Sham, LPS, LPS+EN+OA, LPS+EN+OA+SR202 (SR) and LPS+ pioglitazone (PI) groups to examine whether OA-rich EN alleviated acute liver injury through the PPARγ/STAT-1/MyD88 pathway. Rats received nutrition support via a gastric tube for 3 days. We evaluated the liver histology, apoptosis, liver enzymes and inflammatory cytokine levels in the liver and serum. PPARγ/STAT-1/MyD88 pathway was also measured.
OA-rich EN inhibited the phosphorylation of STAT-1 and the activity of MyD88 by activating PPARγ and alleviating LPS-induced acute liver injury more effectively than EN alone in endotoxemic rats. The use of SR counteracted the effect of OA-rich EN on acute liver injury. Meanwhile, PI showed effects similar to OA-rich EN in endotoxemic rats.
OA-rich EN alleviated acute liver injury through PPARγ/STAT-1/MyD88 pathway in endotoxemic rats.
背景/目的：脓毒症的器官衰竭以急性肝损伤为特征。肠内营养（EN）是脓毒症患者的重要临床治疗措施。然而，单独使用 EN 的治疗效果并不明显。在这里，我们研究了富含辛酸（OA）的 EN 是否通过 PPARγ/STAT-1/MyD88 通路缓解内毒素血症大鼠的急性肝损伤。
首先，大鼠随机分为四组：Sham、脂多糖（LPS）、LPS+EN 和 LPS+EN+OA 组，以研究 OA 丰富的 EN 对内毒素血症大鼠 LPS 诱导的急性肝损伤的影响。然后，大鼠随机分为五组：Sham、LPS、LPS+EN+OA、LPS+EN+OA+SR202（SR）和 LPS+吡格列酮（PI）组，以检查 OA 丰富的 EN 是否通过 PPARγ/STAT-1/MyD88 通路缓解急性肝损伤。大鼠通过胃管接受营养支持 3 天。我们评估了肝组织学、凋亡、肝酶和肝脏及血清中的炎症细胞因子水平。还测量了 PPARγ/STAT-1/MyD88 通路。
OA 丰富的 EN 通过激活 PPARγ，比单独使用 EN 更有效地抑制 STAT-1 的磷酸化和 MyD88 的活性，从而更有效地缓解内毒素血症大鼠的急性肝损伤。使用 SR 抵消了 OA 丰富的 EN 对内毒素血症大鼠急性肝损伤的作用。同时，PI 在脓毒症大鼠中表现出与 OA 丰富的 EN 相似的作用。
OA 丰富的 EN 通过 PPARγ/STAT-1/MyD88 通路缓解内毒素血症大鼠的急性肝损伤。
