Liu Ying, Wei Wenhua, Liang Shiwei, Fang Haicheng, Cao Jie
Department of Gastroenterology, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Department of Radiology, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Evid Based Complement Alternat Med. 2022 Aug 31;2022:7757833. doi: 10.1155/2022/7757833. eCollection 2022.
Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that commonly affects the health of many individuals. Esculentoside A (EsA), a saponin extracted from the roots of , has antioxidative and anti-inflammatory effects against various diseases. Nonetheless, its role in UC is undetermined. Hence, in this study, we examined the therapeutic effects of EsA in UC.
Primary intestinal neuronal cells () were treated with lipopolysaccharide (LPS) to induce inflammatory injury. An UC rat model was created by the administration of dextran sulfate sodium (DSS) to rats, which were subsequently treated with different doses of EsA. The effects of EsA on intestinal motility, histological score, inflammatory response, hydrogen sulfide (HS)/cystathionine -lyase (CSE) system, NO/neuronal nitric oxide synthase (nNOS) system, and LPS-induced primary intestinal neuronal cell viability loss, proliferation inhibition, and apoptosis were detected.
, EsA treatment increased the number of DSS-inhibited bowel movements and body weight, improved the histological score of colitis, and inhibited the inflammatory response by reducing IL-6 and TNF- levels in rats. More importantly, EsA reduced the NO and HS levels in serum and CSE, CBS, and nNOS expressions in the colon tissue. , EsA treatment eased the viability loss, proliferation inhibition, and apoptosis of LPS-stimulated primary intestinal neuronal cells, as well as inhibited the expressions of IL-6, TNF-, CSE, CBS, and nNOS in cells.
EsA improved intestinal motility and suppressed inflammatory response in DSS-induced UC, which may be mediated by HS/CSE and NO/nNOS systems.
溃疡性结肠炎（UC）是一种炎症性肠病（IBD），常影响许多人的健康。从[植物名称]根中提取的皂苷七叶皂苷A（EsA）对多种疾病具有抗氧化和抗炎作用。然而，其在UC中的作用尚不确定。因此，在本研究中，我们检测了EsA对UC的治疗效果。
用脂多糖（LPS）处理原代肠神经元细胞（）以诱导炎症损伤。通过给大鼠施用葡聚糖硫酸钠（DSS）建立UC大鼠模型，随后用不同剂量的EsA进行治疗。检测EsA对肠道运动、组织学评分、炎症反应、硫化氢（HS）/胱硫醚 -裂解酶（CSE）系统、一氧化氮（NO）/神经元型一氧化氮合酶（nNOS）系统以及LPS诱导的原代肠神经元细胞活力丧失、增殖抑制和凋亡的影响。
，EsA治疗增加了DSS抑制的排便次数和体重，改善了结肠炎的组织学评分，并通过降低大鼠体内白细胞介素 -6（IL-6）和肿瘤坏死因子 -（TNF-）水平抑制了炎症反应。更重要的是，EsA降低了血清中的NO和HS水平以及结肠组织中CSE、CBS和nNOS的表达。，EsA治疗减轻了LPS刺激的原代肠神经元细胞的活力丧失、增殖抑制和凋亡，并抑制了细胞中IL-6、TNF-、CSE、CBS和nNOS的表达。
EsA改善了DSS诱导的UC中的肠道运动并抑制了炎症反应，这可能由HS/CSE和NO/nNOS系统介导。
