Abstract
Purpose To assess the preventive effects of acupuncture at back-shu and front-mu acupoints on rats with restraint water-immersion stress (RWIS)-induced gastric ulcer. Methods Thirty-six rats were randomly divided into four groups for 10 days of treatment as follows: the normal group received no treatment; the model group received RWIS-induced gastric ulcer; the omeprazole group was administered omeprazole orally every 2 days; and the electroacupuncture group received electroacupuncture at the RN12 and BL21 acupoints every 2 days. After 10 days of treatment, except for the normal group, all rats were induced with gastric ulcer by RWIS for 3 h. The ulcer index (UI), ulcer inhibition rate, and histopathological score were calculated. We determined the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in serum, and the activities of myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO), and glutathione peroxidase (GSH-Px) in serum and gastric tissues. Protein expression of MyD88, nuclear factor (NF)-κB (p65), and toll-like receptor (TLR) 4 was quantified in gastric tissues. Results The electroacupuncture and omeprazole groups were equivalent in terms of UI, ulcer inhibition rate, and histopathological score. The serum levels of TNF-α and IL-6 were significantly lower in the electroacupuncture group compared with the omeprazole group (P < 0.05). Compared with the model group, there were significant changes in the levels of NO, MPO, GSH-Px, and MDA in all other groups, while the expression of TLR4, MyD88, and NF-κB p65 in gastric tissue decreased significantly in the electroacupuncture group. The expression of TLR4 was substantially lower in the electroacupuncture group compared with the omeprazole group. Conclusion Acupuncture at back-shu and front-mu acupoints played a role in preventing gastric ulcer by inhibiting extracellular signals, stimulating kinases in serum and gastric tissues, and activating the inhibition of the TLR4 signaling pathway.
Highlights
Gastric ulcer is one of the most common digestive diseases but is not cured; those that are cured commonly reoccur. e main causes of this illness are excessive psychological stress, alcohol consumption, smoking, Helicobacter pylori infection, nutritional deficiencies, and frequent use of nonsteroidal anti-inflammatory drugs [1].When homeostasis is disrupted, the adaptive physiological stress response occurs as a mechanism to restore the steady state
GSH-Px further degrades H2O2 produced by superoxide dismutase (SOD) disproportionation [27]. e induction of stress ulcer in the model rats in this study significantly increased MDA and MPO and significantly decreased SOD, GSH-Px, and nitric oxide (NO) compared with normal, untreated rats. ese results indicate that when stress ulcers occur, oxidized substances are increased, while antioxidant substances that could reduce gastric tissue damage are decreased
Research has shown that acupuncture can reduce tumor necrosis factor (TNF)-α and IL-6 levels in serum [31, 32], as well as inhibit the degree of intracellular inflammatory response [33,34,35]. e results of our study showed that the levels of IL-6 and TNF-α were significantly, markedly higher in the model group compared with the normal group, indicating that stress ulceration increases the infiltration of proinflammatory cells
Summary
Gastric ulcer is one of the most common digestive diseases but is not cured; those that are cured commonly reoccur. e main causes of this illness are excessive psychological stress, alcohol consumption, smoking, Helicobacter pylori infection, nutritional deficiencies, and frequent use of nonsteroidal anti-inflammatory drugs [1].When homeostasis is disrupted, the adaptive physiological stress response occurs as a mechanism to restore the steady state. E main causes of this illness are excessive psychological stress, alcohol consumption, smoking, Helicobacter pylori infection, nutritional deficiencies, and frequent use of nonsteroidal anti-inflammatory drugs [1]. Injury to organs and diseases including diabetes can be induced by chronic or severe stress. A classic example of organ injury caused by surgery, trauma, or sepsis is stressinduced gastric ulcer [2]. The precise pathogenesis remains unknown, it is generally acknowledged that stress ulcer development involves the effects of inflammatory responses and oxidation imbalance, the upregulation of proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL), and the generation of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), hydroxyl radical, and superoxide anion. ROS generated by ischemic tissue are considered to be a mediator of stress-induced lesions [10]. ROS induce lipid peroxidation, which subsequently leads to loss of membrane fluidity, weakened membrane integrity, and eventually the loss of cellular functions
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