Medicinal Plants Classification Biosynthesis and ... - Index of

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Aracely E. Chávez-Piña and Andrés Navarrete
Figure 5. Mucus bicarbonate secretion and participation of NO, prostaglandins and non-proteinic
sulfhydryl groups have been describe to participate in triterpenoid-induced gastroprotection mechanism.
Hydrogen sulfide (H 2S), LTB 4 and leukocyte adherence remain unclear.
6. Summary and Conclusions
In summary there are several mechanisms that mediate gastric injury, all of them work
together. PGs are the basis for mucosa gastric defense, they regulate gastric blood flow and
gastric mucus secretion and bicarbonate throw the activation of COX-1; moreover, PGs
regulate leukocyte adherence and reepithelization with COX-2. However, when both
cyclooxygenases are inhibited another mechanism emerges to compensate this lack in PGs
synthesis. NO and H2S are gaseous mediators and it has been elucidated their role in gastric
mucosa defense. Both gases could be synthesized to reduce the damage caused by PGs
inhibition; they share roles with PGs such as the increment in gastric blood flow and the
inhibition on leukocyte adherence.
Ethanol- and NSAIDs-induced gastric injuries are the most common experimental
models for the study of gastroprotective drugs. Ethanol induces mucosa necrosis and NSAIDs
inhibit PGs synthesis to stimulate damage. Furthermore, both increment TNF-α to induce
injury. Several natural products have exhibited a significant contribution in the field of
gastroprotective substances. Triterpenes are compounds with gastroprotective properties; they
play this role by PGs, NO and/or -SH stimulation. There are many reports about the role that
LTB4 plays on gastric damage, however there is not much information about those levels after
administration of gastroprotective triterpenoids.
Moreover, a lack on leukocyte adherence may play a role in the gastroprotective
properties of some triterpenoids. Moreover, there are an unexplored field in the role of
annexins, lipoxins and H2S generation after gastroprotective triterpenoid administration.
TNF-α is another inflammatory mediator that a lack on it should help to the healing of the
endothelium.