Molecular mechanism of astrocyte-related cachexia and pain due to neural invasion of pancreatic cancer

神经系统对神经侵袭（N-inv）的反应可能导致胰腺癌（PCa）的恶病质和疼痛。将Capan-1细胞注入重度联合免疫缺陷小鼠左侧坐骨神经，建立N-inv模型。将N-inv模型与假手术组进行比较。丙烯茶碱（PPF）是一种星形细胞活化抑制剂，每天被注入腹腔。每周测量疼痛和体重（BW）。术后6周对小鼠实施安乐死。在N-inv开始2周后观察到疼痛和星形细胞激活，并在整个实验中保持。体重减少开始于4周，6周时更严重。在N-inv模型中，PPF治疗抑制疼痛、星形细胞激活和体重损失。神经系统对n - invv的反应导致PCa的恶病质。神经系统对n - invv的反应导致PCa的恶病质。

The reaction of the nervous system to neural invasion (N-inv) may lead to cachexia and pain in pancreatic cancer (PCa). The N-inv model was created by injecting Capan-1 cells into the left sciatic nerve of severe combined immunodeficiency mice. The N-inv model was compared to a sham operation group. Propentofylline (PPF), an inhibitor of astrocytic activation, was administered daily into the abdominal cavity. Pain and body weight (BW) were measured weekly. Mice were euthanized 6 weeks after surgery.Pain and astrocytic activation were observed 2 weeks after the start of N-inv and maintained throughout the experiment. Loss of BW began at 4 weeks and was worse at 6 weeks. PPF treatment inhibited pain, astrocytic activation, and BW loss in the N-inv model. The reaction of the nervous system to N-inv leads to cachexia in PCa. The reaction of the nervous system to N-inv leads to cachexia in PCa.