PDF(Pubmed)
Abstract：
UNASSIGNED: Ulcerative colitis is a chronic inflammatory bowel disease (IBD) that causes inflammation and ulcers in the rectum and the innermost layer of the large intestine. Our study aimed to elucidate the ameliorative effect of cetirizine (CTZ) and loratadine (LOR) against acetic acid-induced ulcerative colitis in rats via assessment of the PI3K/p-Akt/Nrf2 signaling pathway and proinflammatory cytokine release.
UNASSIGNED: Thirty-two rats were allocated into four groups (n=8). Group (I) was considered normal control. Acetic acid (AA) was injected intrarectally in groups (2-4). Group (2) was kept untreated. Group (3) was administered CTZ (20 mg/kg/day) for 7 days. Group (4) was administered LOR (10 mg/kg/day) for 7 days.
UNASSIGNED: AA showed severe macroscopic colonic lesions associated with increased ulcer number, area, and severity with significantly elevated PI3K, p-Akt, Nrf2, TNF-α, and IL-6 in colorectal tissue as compared to the normal control group. All the aforementioned indicators were greatly improved by CTZ and LOR therapy.
UNASSIGNED: This is the first study to elucidate the ameliorative effect of CTZ and LOR against AA-induced UC in rats. CTZ and LOR treatment mitigates UC via amelioration of the PI3K/p-Akt/Nrf2 pathway and proinflammatory cytokine release.
UNASSIGNED: Thirty-two rats were allocated into four groups (n=8). Group (I) was considered normal control. Acetic acid (AA) was injected intrarectally in groups (2-4). Group (2) was kept untreated. Group (3) was administered CTZ (20 mg/kg/day) for 7 days. Group (4) was administered LOR (10 mg/kg/day) for 7 days.
UNASSIGNED: AA showed severe macroscopic colonic lesions associated with increased ulcer number, area, and severity with significantly elevated PI3K, p-Akt, Nrf2, TNF-α, and IL-6 in colorectal tissue as compared to the normal control group. All the aforementioned indicators were greatly improved by CTZ and LOR therapy.
UNASSIGNED: This is the first study to elucidate the ameliorative effect of CTZ and LOR against AA-induced UC in rats. CTZ and LOR treatment mitigates UC via amelioration of the PI3K/p-Akt/Nrf2 pathway and proinflammatory cytokine release.
摘要：
■溃疡性结肠炎是一种慢性炎症性肠病（IBD），可引起直肠和大肠最内层的炎症和溃疡。我们的研究旨在通过评估PI3K/p-Akt/Nrf2信号通路和促炎细胞因子释放，阐明西替利嗪（CTZ）和氯雷他定（LOR）对大鼠乙酸诱导的溃疡性结肠炎的改善作用。
■将32只大鼠分成4组(n=8)。组(I)为正常对照。组(2-4)直肠内注射乙酸(AA)。组(2)保持未处理。组(3)施用CTZ(20mg/kg/天)7天。组(4)施用LOR(10mg/kg/天)7天。
■AA显示严重的宏观结肠病变与溃疡数量增加有关，area,严重程度与PI3K显著升高，p-Akt,Nrf2,TNF-α,与正常对照组相比，结直肠组织中的IL-6。CTZ和LOR治疗对上述各项指标均有较大改善。
■这是首次阐明CTZ和LOR对AA诱导的大鼠UC的改善作用的研究。CTZ和LOR治疗通过改善PI3K/p-Akt/Nrf2途径和促炎细胞因子释放减轻UC。
■将32只大鼠分成4组(n=8)。组(I)为正常对照。组(2-4)直肠内注射乙酸(AA)。组(2)保持未处理。组(3)施用CTZ(20mg/kg/天)7天。组(4)施用LOR(10mg/kg/天)7天。
■AA显示严重的宏观结肠病变与溃疡数量增加有关，area,严重程度与PI3K显著升高，p-Akt,Nrf2,TNF-α,与正常对照组相比，结直肠组织中的IL-6。CTZ和LOR治疗对上述各项指标均有较大改善。
■这是首次阐明CTZ和LOR对AA诱导的大鼠UC的改善作用的研究。CTZ和LOR治疗通过改善PI3K/p-Akt/Nrf2途径和促炎细胞因子释放减轻UC。
