Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Republic of Korea.
Department of Anesthesiology and Pain Medicine, Kyung Hee Medical Center, College of Medicine, Kyung Hee University, Seoul, Republic of Korea.
Biomed Res Int. 2020 Feb 21;2020:2169083. doi: 10.1155/2020/2169083. eCollection 2020.
Ischemic colitis is resulted from an inadequate blood supply to a segment or entire colon. Polydeoxyribonucleotide (PDRN), extracted from salmon sperm, has been reported to exert anti-inflammatory and anti-ischemic effects through the adenosine A receptor (AR). We investigated whether PDRN possesses therapeutic effectiveness on ischemic colitis rats. Ischemic colitis was induced by selective devascularization. The skin temperature on the ischemic colitis-induced region was determined. To assess the colonic damage score and collagen deposition, colonic tissue sections were stained with hematoxylin and eosin (H&E), and Masson trichrome staining was performed. Western blot analysis for AR, vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), tumor necrosis factor- (TNF-), interleukin-1 (IL-1), and IL-6, Bax, Bcl-2, and extracellular signal-regulated kinase 1/2 (ERK1/2) was performed. Skin temperature was increased and mucosal damage and collagen deposition were observed in the affected colonic tissues in the ischemic colitis rats. Expressions of inflammatory cytokines (TNF-, IL-1, and IL-6) and inflammatory mediator (COX-2) were upregulated in the ischemic colitis rats. Apoptosis was increased by decreasing the ratio of Bcl-2 to Bax and by suppressing the phosphorylated form of ERK1/2 expression in the ischemic colitis rats. Treatment with PDRN alleviated mucosal damage reduced the expressions of inflammatory cytokines and COX-2 and inhibited apoptosis in the ischemic colitis rats. PDRN treatment more enhanced the expressions of AR and VEGF in the ischemic colitis rats. PDRN showed therapeutic effectiveness on ischemic colitis by increasing VEGF expression and inhibiting inflammatory cytokines and COX-2 through enhancing AR expression.
缺血性结肠炎是由于一段或整个结肠的血液供应不足引起的。多聚脱氧核苷酸(PDRN)是从三文鱼精子中提取的,据报道,它通过腺苷 A 受体(AR)发挥抗炎和抗缺血作用。我们研究了 PDRN 是否对缺血性结肠炎大鼠具有治疗效果。通过选择性去血管化诱导缺血性结肠炎。测定缺血性结肠炎诱导区域的皮肤温度。为了评估结肠损伤评分和胶原沉积,用苏木精和伊红(H&E)染色结肠组织切片,并进行 Masson 三色染色。进行 AR、血管内皮生长因子(VEGF)、环氧化酶-2(COX-2)、肿瘤坏死因子-(TNF-)、白细胞介素-1(IL-1)和 IL-6、Bax、Bcl-2 和细胞外信号调节激酶 1/2(ERK1/2)的 Western blot 分析。在缺血性结肠炎大鼠中,皮肤温度升高,受影响的结肠组织中的粘膜损伤和胶原沉积。在缺血性结肠炎大鼠中,炎症细胞因子(TNF-、IL-1 和 IL-6)和炎症介质(COX-2)的表达上调。通过降低 Bax 与 Bcl-2 的比值和抑制 ERK1/2 表达的磷酸化形式,缺血性结肠炎大鼠中的细胞凋亡增加。PDRN 治疗减轻了粘膜损伤,降低了炎症细胞因子和 COX-2 的表达,并抑制了缺血性结肠炎大鼠的细胞凋亡。PDRN 治疗通过增加 AR 和 VEGF 的表达,抑制炎症细胞因子和 COX-2,从而对缺血性结肠炎大鼠具有治疗效果。