Dissertation > Medicine, health > Pharmacy > Pharmacology

The protective effect of the new gaseous signal molecule of non-steroidal anti-inflammatory drug -induced gastric lesions

Author CaiZuo
Tutor XuGuangLin
School Nanjing Normal University
Course Physiology
Keywords hydrogen sulfide diclofenac sodium gastric injury MAPK
Type Master's thesis
Year 2011
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Hydrogen sulfide (H2S) has been suggested as a gaseous mediator in mammals and became the third gaseous transmitter after NO and CO; however the role of H2S in the regulation of anti-inflammatory activity and gastric injury of NSAIDs is far from being understood completely. We focused on the role of H2S on the inflammatory and investigated the effect of H2S on gastric injury caused by diclofenac sodium, focusing on the morphological features of gastric injury. Furthermore, we research molecular mechanism of gastric injury.1. The role of H2S on the inflammatoryFirst we used xylene-induced mouse ear swelling——the classic inflammation model to study H2S in vivo anti-inflammatory activity. The results showed that H2S has a strong anti-inflammatory activity in vivo. At the same time H2S can enhance the anti-inflammatory activity significantly.2. Observation of the role of NaHS through morphological aspectsWe observed the role of NaHS through three morphological aspects such as macroscopical observation and observation under light microscope and transmission electron microscope, through the morphological observation of gastric mucosa we can obtain the result that NaHS can protect the gastric injury caused by NSAIDs. Macroscopical observation showed that NaHS could alleviate bleeding and erosion. The pathological examination of HE-stained slides of gastric mucosa showed that rats treated with NaHS had slight lamina propria congestion, edema. Further ultrastructure examination showed that NaHS protected the integrity of cells.3. Molecular mechanism of protection of H2S on gastric injuryOur results suggest that orally administration of NaHS has a protective effect on gastric mucosal injury caused by diclofenac sodium which might be related to the regulation of expression of CSEmRNA, CBSmRNA and the molecular mechanism might be related to the activation of phosphorylation of mitogen-activated protein kinases (MAPK) pathways.In conclusion, our research suggested that H2S has significant anti-inflammatory effect in mice, and has a protection effect on gastric injury caused by NSAIDs, in which the molecular mechanism the mechanism may be related to activation of ERKl/2 MAPK signaling pathway kinases.

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