Title Page
Contents
ABSTRACT 8
I. INTRODUCTION 10
II. MATERIALS AND METHODS 13
1. Tissue preparation 13
2. Ethanol/Hydrochloride (Et/HCl)-induced gastric ulcer 13
3. Histological analysis 14
4. Assessment of cAMP 14
5. Evaluation of the role of nitric oxide (NO), KATP channel, prostaglandin and transient potential vanilloid 1 (TRPV1)(이미지참조) 14
6. Evaluation of lipid peroxidation 15
7. Data analysis 16
III. RESULTS 17
1. Effect of MN-1695 on the gastric damage induced by Et/HCl 17
2. Synergic effects of MN-1695 and SNAP on cAMP content 17
3. Effects of L-arginine and L-NAME on MN-1695-induced gastroprotection 20
4. Effects of gibenclamide and diazoxide on MN-1695-induced gastroprotection 20
5. Effects of capsazepine and indomethacin pretreatments on MN-1695-induced gastroprotection 20
6. Effect of MN-1695 on gastric mucosal TBARS content 25
IV. DISCUSSION 27
V. CONCLUSION 31
REFERENCES 32
ABSTRACT(Korean) 38
Fig. 1. Photomicrophs of HE staining of gastric mucosa (maganification × 40). 18
Fig. 2. Elevation of intracellular cAMP content by MN-1695 and SNAP. 19
Fig. 3. Involvement of nitric oxide in the gastroprotection of MN-1695 in mice subjected to Et/HCl-induced gastric damage. 21
Fig. 4. Effects of the pretreatment with glibenclamide on the gastroprotection of MN-1695 in mice subjected to Et/HCl-induced gastric damage. 22
Fig. 5. Role of vanilloid receptors (TRPV1) on the gastroprotection of MN-1695 in mice subjected to Et/HCl-induced gastric damage. 23
Fig. 6. Effect of pretreatment with indomethacin on the gastroprotection of MN-1695 in mice subjected to Et/HCl-induced gastric ulceration. 24
Fig. 7. Effect of MN-1695 on lipid peroxidation (TBARS) in mice stomach homogenates. 26