Effect of moxibustion treatment on cell apoptosis and expressions of heat shock protein and second mitochondrial activator of caspase in acute gastric mucosal lesion of rats

Yu, Jie; Peng, Hong; Lin, Yaping; Yi, Shuhua

doi:10.1016/s0254-6272(13)60136-3

Cited by 11 publications

(6 citation statements)

References 3 publications

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“…It might induce a series of signal pathways and stress through heat shock proteins [22, 39], including the Akt pathway and ER stress, as shown in the present study. Although the effect of moxibustion in the whole body requires more evidence, moxibustion is a suitable technique for local heat therapy to stimulate self-healing, recovery, and innate defense mechanisms.…”

Section: Discussionmentioning

confidence: 59%

Moxibustion Activates Macrophage Autophagy and Protects Experimental Mice against Bacterial Infection

Guo

Shen

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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Moxibustion is one of main therapies in traditional Chinese medicine and uses heat stimulation on the body surface from the burning of moxa to release pain or treat diseases. Emerging studies have shown that moxibustion can generate therapeutic effects by activating a series of signaling pathways and neuroendocrine-immune activities. Here we show moxibustion promoted profound macrophage autophagy in experimental Kunming mice, with reduced Akt phosphorylation and activated eIF2α phosphorylation. Consequently, moxibustion promoted bacterial clearance by macrophages and protected mice from mortality due to bacterial infection. These results indicate that moxibustion generates a protective response by activating autophagy against bacterial infections.

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Section: Discussionmentioning

confidence: 59%

Moxibustion Activates Macrophage Autophagy and Protects Experimental Mice against Bacterial Infection

Guo

Shen

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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“…Caspase-3 is a key mediator for apoptosis and Liu et al [34] determined that caspase-3 is play in apoptotic cell death in stress-induced ulcer rat model. Some studies have shown that caspase 3 expression has increased in experimentally gastric ulcer models [35][36][37][38]. We detected that IND induced to apoptosis by increasing caspase-3 expression in stomach tissue and NA administration prevented to this evaluate in caspase-3 expression.…”

Section: Discussionmentioning

confidence: 57%

Protective effects of naringin in indomethacin-induced gastric ulcer in rats

Şengül¹,

Gelen²

2019

GSC Biol. and Pharm. Sci.

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This study aimed to investigate the potential protective effects of Naringin (NA) in Indomethacin (IND)-induced gastric ulcers in rats. Forty adult male Sprague Dawley rats were randomly divided into four groups; the control group was given intragastric (ig) saline for 10 days, the IND group was given ig saline for 10 days and given a single dose of IND (100 mg/kg, ig) on the 11th day, and the NA+IND and RAN+IND groups were administered NA (100 mg/kg, ig) and RAN (5mg/kg, ig) for 10 days, respectively. These final two groups were administered single dose IND (100 mg/kg, ig) on the 11th day, and 24 hours after IND administration, the rats were decapitated under anesthesia. The stomach tissues were examined to calculate the ulcer index and analyze inflammation and apoptosis markers. In addition, microscopic examination of the stomach tissues was performed. The results showed that IND induced gastric ulcers and increased tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), inducible nitric oxide synthase (iNOS), and caspase-3 levels while decreasing cyclooxygenase-2 (COX-2). NA exhibited a protective effect by preventing these parameter changes. In addition, NA corrected the histopathological abnormalities caused by IND in stomach tissue. These results indicate that NA might protect against the effects of IND in rats.

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“…In general, apoptosis is a type of organized cell self-destruction by a series of signal cascades that include numerous gene products and cytokines. Caspase-3 activation serves an important role in apoptosis, whilst the imbalance between Bcl-2 (anti-apoptotic) and Bax (pro-apoptotic) has been recognized as a signature of the acquisition of apoptosis resistance in cancer cells ( 42 , 43 ). In addition, p53, acting as a transcriptional factor, serves an important role in promoting apoptosis in response to various cellular stressors, including oncogene activation ( 44 ).…”

Section: Discussionmentioning

confidence: 99%

Pro‑apoptotic effects of Kangfuxin on human stomach cancer cells and its underlying mechanism

Ma¹,

Sun

et al. 2018

Oncol Lett

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Kangfuxin (KFX) is an oral liquid derived from Periplaneta americana, with complex components. KFX has been demonstrated to exhibit anticancer activity in a variety of different types of tumor, including gastric cancer; however, its underlying molecular mechanism remains unclear. The present study was designed to investigate the pro-apoptotic effects of KFX on SGC-7901 cells, in order to provide a theoretical basis for clinical application. In order to clarify the pro-apoptotic effects of KFX on SGC-7901 cells, MTT analysis was conducted. To evaluate the anticancer effect of KFX, peroxisome proliferator-activated receptor (PPAR)-γ was analyzed by reverse transcription-polymerase chain reaction. Western blot analysis was used to determine the effects of KFX on the expression of cleaved caspase-3, phosphorylated extracellular signal-regulated kinase (p-ERK), ERK, tumor protein p53 (p53), B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X, interleukin (IL)-6 and IL-1β. In addition, terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling (TUNEL) analysis was used to detect apoptosis in SGC-7901 cells. It was revealed that PPAR-γ was increased in SGC-7901 cells following treatment with KFX, shown by an increase in mRNA expression. Furthermore, western blot analysis identified that KFX treatment groups exhibited markedly inhibited levels of Bcl-2, IL-6, IL-1β and p-ERK, and induced p53 protein expression. Additionally, TUNEL and MTT assays demonstrated that treatment with KFX may induce SGC-7901 cell apoptosis and inhibit proliferation. In conclusion, to the best of our knowledge, the results of the present study demonstrated for the first time that KFX may induce SGC-7901 cell apoptosis and inhibit its proliferation, and this may be primarily attributed to its role in mitogen-activated protein kinase/extracellular-signal-regulated kinase kinase/ERK signaling pathway inhibition.

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Effect of moxibustion treatment on cell apoptosis and expressions of heat shock protein and second mitochondrial activator of caspase in acute gastric mucosal lesion of rats

Abstract: The moxibustion treatment could alleviate the gastric mucosal lesion caused by anhydrous ethanol, induce the over-expressions of HSP60 and HSP70, and down-regulate the expression of Smac, which could suppress cell apoptosis.

Cited by 11 publications

References 3 publications

Moxibustion Activates Macrophage Autophagy and Protects Experimental Mice against Bacterial Infection

Moxibustion Activates Macrophage Autophagy and Protects Experimental Mice against Bacterial Infection

Protective effects of naringin in indomethacin-induced gastric ulcer in rats

Pro‑apoptotic effects of Kangfuxin on human stomach cancer cells and its underlying mechanism

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