Objectives: The gastric ulcer is a common disorder of the stomach and duodenum. The basic physiopathology of a gastric ulcer results from an imbalance between some endogenous aggressive and cytoprotective factors. This study examined whether Ganoderma lucidum pharmacopuncture (GLP) would provide pro...
Objectives: The gastric ulcer is a common disorder of the stomach and duodenum. The basic physiopathology of a gastric ulcer results from an imbalance between some endogenous aggressive and cytoprotective factors. This study examined whether Ganoderma lucidum pharmacopuncture (GLP) would provide protection against acute gastric ulcers in rats. Methods: Sprague-Dawley rats were divided randomly into 4 groups of 8 rats each: normal, control, normal saline (NP) and GLP groups. The experimental acute gastric ulcer was induced by using an EtOH/HCl solution and the normal group received the same amount of normal saline instead of ethanol. The NP and the GLP groups were treated once with injections of saline and GLP, respectively. Two local acupoints were used: CV12 (中脘) which is the alarm point of the Stomach Meridian, and ST36 (足三里), which is the sea point of the Stomach Meridian. The stomachs from the rats in each group were collected and analyzed for gross appearance and histology. Also, immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$ was performed. Results: Histological observations of the gastric lesions in the control group showed comparatively extensive damage of the gastric mucosa and necrotic lesions had penetrated deeply into the mucosa. The lesions were long, hemorrhagic, and confined to the glandular portions. The lesions were measured microscopically by using the clear depth of penetration into the gastric mucosal surface. The length and the width of the ulcer were measured and the inhibition percentage was calculated. Wound healing of the acute gastric ulcer was promoted by using GLP, and significant alterations of indices in gastric mucosa were observed. Such protection was shown by gross appearance, histology and immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$. Conclusion: These results suggest that GLP administered at CV12 and ST36 can provide significant protection to the gastric mucosa against an ethanol-induced acute gastric ulcer.
Objectives: The gastric ulcer is a common disorder of the stomach and duodenum. The basic physiopathology of a gastric ulcer results from an imbalance between some endogenous aggressive and cytoprotective factors. This study examined whether Ganoderma lucidum pharmacopuncture (GLP) would provide protection against acute gastric ulcers in rats. Methods: Sprague-Dawley rats were divided randomly into 4 groups of 8 rats each: normal, control, normal saline (NP) and GLP groups. The experimental acute gastric ulcer was induced by using an EtOH/HCl solution and the normal group received the same amount of normal saline instead of ethanol. The NP and the GLP groups were treated once with injections of saline and GLP, respectively. Two local acupoints were used: CV12 (中脘) which is the alarm point of the Stomach Meridian, and ST36 (足三里), which is the sea point of the Stomach Meridian. The stomachs from the rats in each group were collected and analyzed for gross appearance and histology. Also, immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$ was performed. Results: Histological observations of the gastric lesions in the control group showed comparatively extensive damage of the gastric mucosa and necrotic lesions had penetrated deeply into the mucosa. The lesions were long, hemorrhagic, and confined to the glandular portions. The lesions were measured microscopically by using the clear depth of penetration into the gastric mucosal surface. The length and the width of the ulcer were measured and the inhibition percentage was calculated. Wound healing of the acute gastric ulcer was promoted by using GLP, and significant alterations of indices in gastric mucosa were observed. Such protection was shown by gross appearance, histology and immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$. Conclusion: These results suggest that GLP administered at CV12 and ST36 can provide significant protection to the gastric mucosa against an ethanol-induced acute gastric ulcer.
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가설 설정
In particular, there are no reports of the gastroprotective effect of GLP against ethanol-induced gastric mucosal lesions. Because ethanol-induced gastric mucosal lesions are mediated by the generation of free radicals, we hypothesized that GLP might inhibit ethanol-induced gastric mucosal lesions through a protective effect that might directly involve its antioxidant property. Therefore, this study was designed to investigate the gastroprotective effect of GLP by measuring the amount of lipid peroxidation and by comparing the activities of the SOD enzyme.
The length and the width of the ulcer were measured, and the inhibition percentage was calculated. We hypothesized that GLP could inhibit ethanol-induced gastric mucosal lesions, and that such protective effects might directly involve its antioxidant property. We investigated the effect of GLP on the activities of the radical scavenging enzymes, SOD, in the gastric mucosa.
제안 방법
In this study, gastric mucosal lesions in rats were induced by using EtOH/HCl for an acute injury model. Animals were treated with GLP or NP and were kept under observation for 1 hour, during which time they remained alive.
In this study, to investigate the effects of GLP on the ability to repair gastric ulcer damage, we carried out an immunohistochemical analysis of TGF-β1 in rats with ethanol-induced acute gastric ulcers (Fig. 8, 9).
Ulcers of the gastric mucosa appear as elongated bands of hemorrhagic lesions parallel to the long axis of the stomach. The gastric mucosa of each rat was examined in order to estimate damage. The length and the width of the ulcer (mm) were measured.
They were provided with standard food and water ad libitum and were maintained in an animal house at a controlled temperature (22 ± 2℃) with a 12-hours light/dark cycle. The rats were divided randomly into 4 groups of 8 rats each: normal, control, normal saline (NP) and GLP groups. The study was approved by the Ethics Committe for Animal Experimentation, DongEui University.
Next, the biopsy samples were embedded in paraffin wax, sectioned into 5-μm thicknesses by using a microtome, and then stained with hematoxylin and eosin (H&E). The tissue sections were assessed for histopathological changes such as congestion, edema, hemorrhage and necrosis by using a light microscope.
Because ethanol-induced gastric mucosal lesions are mediated by the generation of free radicals, we hypothesized that GLP might inhibit ethanol-induced gastric mucosal lesions through a protective effect that might directly involve its antioxidant property. Therefore, this study was designed to investigate the gastroprotective effect of GLP by measuring the amount of lipid peroxidation and by comparing the activities of the SOD enzyme.
To confirm the effect of GLP against ethanol-induced acute gastric ulcers, gastric ulcer lesions were measured microscopically by using the clear depth of penetration into the gastric mucosal surface in all experimental groups except the normal group (Fig. 3). The length and the width of the ulcer were measured, and the inhibition percentage was calculated.
데이터처리
Es). The statistical significance of differences among groups were assessed with the one-way ANOVA (post-hoc analysis). A value of P < 0.
성능/효과
This study revealed that GLP can significantly protect the gastric mucosa against an ethanol-induced gastric ulcer. Such protection was shown by gross appearance, histology, and immunohistochemistry staining for BAX, Bcl-2 and TGF-β1.
참고문헌 (20)
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