ABSTRACT
Objective To study the effect of APETx2 on the expression of ASIC3 APETx2 in a rat model of acute gastric mucosal lesion(AGML). Methods Twenty-four Wistar rats were randomly assigned to three groups in equal number : normal control group, water immersion restraint stress (WIRS) group, APETx2 treatment group. AGML was induced by WIRS for 6 hours, and APETx2 (25 μg/kg) was injected intraperitoneally before the onset of stress. Intragastric pH and gastric histopathological changes were measured and the expression of ASIC3 mRNA in DRG neurons projecting to rat stomach was examined by real-time PCR. Immunohistochemistry was performed to detect the localization of ASIC3. Results Compared with the normal control group, the WIRS group showed obvious gastric injury with lower values of intragastric pH and extensive expression of ASIC3 in the DRG neurons (P < 0.05). The treatment with APETx2 before the onset of WIRS significantly alleviated the gastric mucosal injury, decreased gastric acidity and reduced ASIC3 expression in DRG neurons (P < 0.05). Conclusions ASIC3 expression in DRG neurons projecting to rat stomach is strongly associated with gastric mucosal lesion and acidosis in the WIRS model. APETx2 can improve gastric acidosis and prevent the occurrence of these lesions.
ABSTRACT
Objective To investigate the effects of restraint stress (RS) in different periods on SOD and MDA of normal rat serums and mucosal tissues. Methods 32 adult male Wistar rats were randomly divided into normal control group (NC group, n=8), and restraint stress groups of 3 days, 5 days and 7 days (RS3, RS5 and RS7 groups, n=8 at each group). The comparisons were done between all the groups in terms of the general extent of gastric mucosal injury, gastric mucosal injury ulcer index (UI), water content, the activity of super oxide dismutase (SOD), and the level of malondialdehyde (MDA) in serum and mucosal. Results Compared with NC group, gastric mucosal injuries in RS group were more severe, the UI and water content was proportionally related with the restraint periods. Meanwhile, the serum and mucosal SOD in the RS groups were all increased, and with prolonged restraints, the SOD were decreased, but the serum and mucosal MDA were increased (P<0.01) and SOD/MDA in the mucosa lowered as well (P<0.01). Conclusion Restraint stress may cause mucosal injury proportional to the stress time and related with lowered SOD/MDA in mucosal tissues.
ABSTRACT
Objective To observe the protective effect of sufentanil pretreatment on the rats with acute gastric mucosa lesion (AGML) induced by water immersion and restrain stress (WIRS) and its effect on TRPV1 mRNA expression in the hypothalamus and gastric mucosa. Methods Thirty male Wistar rats were randomly designed into 3 groups, including the normal control group (Group NC, n = 10), the group treated with WRIS for 6 h (Group WIRS, n = 10) and the group pretreated with sufentanil (Group SF, n = 10). The model of AGML was established by the classic WIRS method , and observed for the general extent of gastric mucosal injury at WIRS for 6 hr, and calculated gastric mucosal injury ulcer index (UI) and the PH value of gastric juice; The quantification of TRPV1 mRNA expression in hypothalamus and gastric mucosa was performed using quantitative real-time PCR; In addition, the activity of super oxide dismutase (SOD) and the level of malondialdehyde (MDA) in serum were detected. Results Compared with group NC, gastric mucosal in Group WIRS was injured more seriously , and the UI and the activity of MDA were also obviously increased , but the change of SOD activity was not apparent; The TRPV1 expression in gastric mucosal decreased apparently. Sufentanil pretreatment could effectively relieve gastric mucosal injury induced by WIRS , and make the UI and the activity of MDA decreased , and up-regulate TRPV1 mRNA expression in the hypothalamus and gastric mucosa. Conclusions Sufentanil pretreatment can effectively relieve AGML induced by WIRS , which may be related to the control of oxidative stress response , the reduced gastric acid secretion , and the upregulation of the TRPV1 mRNA expression in the central and periphera nerve.