Natural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, China.
College of Animal Science and Technology, Sichuan Agricultural University, Chengdu, 611130, China.
J Ethnopharmacol. 2024 May 10;325:117845. doi: 10.1016/j.jep.2024.117845. Epub 2024 Feb 1.
The rhizome of Kaempferia galanga L., a medicinal and edible Plant, was widely distributed in many Asian and African counties. It has been traditionally used to treat gastroenteritis, hypertension, rheumatism and asthma. However, there is a lack of modern pharmacology studies regarding its anti-gastric ulcer activity.
The objective of this study is to investigate the protective effects of an extract from K. galanga L. rhizome (Kge) and its active components kaempferol and luteolin on ethanol-induced gastric ulcer.
The kge was prepared by ultrasonic-assisted extraction, and the contents of kaempferol and luteolin were determined by HPLC. The mice were randomly divided into seven groups: blank control (0.5 % CMC-Na; 0.1 mL/10 g), untreatment (0.5 % CMC-Na; 0.1 mL/10 g), Kge (100, 200 and 400 mg/kg), kaempferol (100 mg/kg) and luteolin (100 mg/kg) groups. The mice were treated intragastrically once daily for 7 days. At 1 h post the last administration, the mice in all groups except the blank control group were intragastrically administrated with anhydrous alcohol (0.1 mL/10 g) once to induce gastric ulcer. Then, fasting was continued for 1 h, followed by sample collection for evaluation by enzyme-linked immunosorbent assay and real-time reverse transcription polymerase chain reaction assay.
The contents of kaempferol and luteolin in Kge were determined as 3713 μg/g and 2510 μg/g, respectively. Alcohol induced severely damages with edema, inflammatory cell infiltration and bleeding, and the ulcer index was 17.63 %. After pre-treatment with Kge (100, 200 and 400 mg/kg), kaempferol and luteolin, the pathological lesions were obviously alleviated and ulcer indices were reduced to 13.42 %, 11.65 %, 6.54 %, 3.58 % and 3.85 %, respectively. In untreated group, the contents of Ca, myeloperoxidase, malondialdehyde, NO, cyclic adenosine monophosphate and histamine were significantly increased, while the contents of hexosamine, superoxide dismutase, glutathione peroxidase, and prostaglandin E2 were significantly decreased; the transcriptional levels of IL-1α, IL-1β, IL-6, calcitonin gene related peptide, substance P, M3 muscarinic acetylcholine receptor, histamine H2 receptor, cholecystokinin 2 receptor and H/K ATPase were significantly increased when compared with the blank control group. After pre-treatment, all of these changes were alleviated, even returned to normal levels. Kge exhibited anti-gastric ulcer activity and the high dose of Kge (400 mg/kg) exhibited comparable activity to that of kaempferol and luteolin.
The study showed that K. galanga L., kaempferol, and luteolin have protective effects against ethanol-induced gastric ulcers. This is achieved by regulating the mucosal barrier, oxidative stress, and gastric regulatory mediators, as well as inhibiting the TRPV1 signaling pathway and gastric acid secretion, ultimately reducing the gastric ulcer index.
姜黄属植物的根茎，一种药用和食用植物，广泛分布于许多亚洲和非洲国家。它在传统上被用于治疗胃肠炎、高血压、风湿和哮喘。然而，关于其抗胃溃疡活性的现代药理学研究还很缺乏。
本研究旨在探讨姜黄根茎提取物（Kge）及其活性成分山奈酚和木樨草素对乙醇诱导的胃溃疡的保护作用。
采用超声辅助提取法制备 Kge，采用高效液相色谱法测定山奈酚和木樨草素的含量。将小鼠随机分为七组：空白对照组（0.5% CMC-Na；0.1 mL/10 g）、未处理组（0.5% CMC-Na；0.1 mL/10 g）、Kge（100、200 和 400 mg/kg）、山奈酚（100 mg/kg）和木樨草素（100 mg/kg）组。小鼠每天灌胃一次，连续 7 天。末次给药后 1 h，除空白对照组外，所有组的小鼠均一次性灌胃无水乙醇（0.1 mL/10 g），诱导胃溃疡。然后禁食 1 h，收集样本，通过酶联免疫吸附试验和实时逆转录聚合酶链反应试验进行评估。
Kge 中山奈酚和木樨草素的含量分别为 3713 μg/g 和 2510 μg/g。酒精诱导严重损伤，伴有水肿、炎症细胞浸润和出血，溃疡指数为 17.63%。经 Kge（100、200 和 400 mg/kg）、山奈酚和木樨草素预处理后，病理损伤明显减轻，溃疡指数分别降低至 13.42%、11.65%、6.54%、3.58%和 3.85%。在未处理组中，钙、髓过氧化物酶、丙二醛、NO、环磷酸腺苷和组氨酸的含量显著增加，而己糖胺、超氧化物歧化酶、谷胱甘肽过氧化物酶和前列腺素 E2的含量显著降低；白细胞介素-1α、白细胞介素-1β、白细胞介素-6、降钙素基因相关肽、P 物质、M3 毒蕈碱乙酰胆碱受体、组胺 H2 受体、胆囊收缩素 2 受体和 H/K ATPase 的转录水平与空白对照组相比显著升高。预处理后，所有这些变化均得到缓解，甚至恢复正常水平。Kge 表现出抗胃溃疡活性，高剂量 Kge（400 mg/kg）的活性与山奈酚和木樨草素相当。
本研究表明，姜黄属植物、山奈酚和木樨草素对乙醇诱导的胃溃疡具有保护作用。这是通过调节黏膜屏障、氧化应激和胃调节介质，以及抑制 TRPV1 信号通路和胃酸分泌来实现的，最终降低了胃溃疡指数。
