■在传统医学中,MachiluszuihoensisHayata树皮(MZ)与其他药物联合用于治疗胃癌,胃溃疡(GU),肝脏和心血管疾病。本研究旨在评估MZ粉对酸性乙醇(AE)诱导的GU的胃保护作用和可能的机制及其对小鼠的毒性。
通过在AE诱导GU之前连续14天口服MZ来分析MZ粉末的胃保护作用。计算溃疡指数(UI)和保护百分比,进行苏木精和曙红染色和高碘酸希夫染色,测量胃粘液重量。抗氧化,抗炎,和抗凋亡机制,并对可能的信号通路进行了研究。
■用MZ(100和200mg/kg)预处理显着降低了10μL/gAE引起的粘膜出血,水肿,炎症,和UI,导致88.9%和93.4%的保护百分比,分别。MZ预处理通过降低丙二醛水平和恢复超氧化物歧化酶活性来降低AE诱导的氧化应激。MZ预处理通过降低血清和胃肿瘤坏死因子-α显示抗炎作用,白细胞介素(IL)-6和IL-1β水平。此外,MZ预处理通过降低Bcl-2相关X蛋白/B细胞淋巴瘤2的比例而表现出抗凋亡作用。MZ的胃保护机制涉及活化B细胞的核因子κ轻链增强子(NF-κB)和丝裂原活化蛋白激酶(MAPK)信号通路的失活。否则,200mg/kgMZ不引起肝或肾毒性。总之,MZ通过粘液分泌保护AE诱导的GU,抗氧化,抗炎,和抗凋亡机制,并抑制NF-κB和MAPK信号通路。
UNASSIGNED: In traditional medicine, Machilus zuihoensis Hayata bark (MZ) is used in combination with other medicines to treat gastric cancer, gastric ulcer (GU), and liver and cardiovascular diseases. This study aims to evaluate the gastroprotective effects and possible mechanism(s) of MZ powder against acidic ethanol (AE)-induced GU and its toxicity in mice.
UNASSIGNED: The gastroprotective effect of MZ powder was analyzed by orally administering MZ for 14 consecutive days before AE-inducing GU. Ulcer index (UI) and protection percentage were calculated, hematoxylin and eosin staining and periodic acid-Schiff staining were performed, and gastric mucus weights were measured. The antioxidative, anti-inflammatory, and anti-apoptotic mechanisms, and possible signaling pathway(s) were studied.
UNASSIGNED: Pretreatment with MZ (100 and 200 mg/kg) significantly decreased 10 μL/g AE-induced mucosal hemorrhage, edema, inflammation, and UI, resulted in protection percentages of 88.9% and 93.4%, respectively. MZ pretreatment reduced AE-induced oxidative stress by decreasing malondialdehyde level and restoring superoxide dismutase activity. MZ pretreatment demonstrated anti-inflammatory effects by reducing both serum and gastric tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels. Furthermore, MZ pretreatment exhibited anti-apoptotic effect by decreasing Bcl-2 associated X protein/B-cell lymphoma 2 ratio. The gastroprotective mechanisms of MZ involved inactivations of nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) and mitogen activated protein kinase (MAPK) signaling pathways. Otherwise, 200 mg/kg MZ didn\'t induce liver or kidney toxicity. In conclusion, MZ protects AE-induced GU through mucus secreting, antioxidative, anti-inflammatory, and anti-apoptotic mechanisms, and inhibitions of NF-κB and MAPK signaling pathways.