RESUMO
Background: Gastric cancer is one of the most significant reasons for cancer-related death. miR-146a is one of the dysregulated factors associated with gastric tumorigenesis. However, deregulation of this microRNA (miRNA) has become controversial. Moreover, the inflammation-mediating role of this miRNA implies that miR-146a might be dysregulated by gastric cancer-related pathogens, such as Helicobacter pylori. However, the dysregulation of miR-146a in H. pylori-infected gastric tumors has not been widely studied. Objectives: We aimed to analyze the expression level of miR-146a in gastric cancer tissues and then to assess any potential association between miR-146a and H. pylori infection and other clinical characteristics. Materials and Methods: miR-146a expression level was quantitatively studied by reverse transcription quantitative polymerase chain reaction, in 144 fresh tissues including 44 normal and 100 gastric cancer samples. Results: A dramatic overexpression of miR-146a was observed in primary gastric tumors. miR-146a showed lower expression in progressed tumors with greater stages and lymph node metastasis. Conclusion: miR-146a is highly expressed in primary gastric tumor independent of H. pylori infection. It is highly expressed in the lower stages and lymph node-negative tumors. It might suggest the importance of upregulation and downregulation of this miRNA in the initiating/promoting and progressive steps of gastric tumorigenesis, respectively
RESUMO
Hypomagnesemia is one of the nephrotoxicity signs. In addition, renin-angiotensin system may be involved in pathophysiology of kidney diseases. Therefore, the present study was designed to investigate the possible role of losartan plus oral magnesium sulfate (MgSO4) to reduce CP-induced nephrotoxicity in female rats. The animals were divided into twelve groups: Group 1-6 received saline, MgSO4 (3g/l), MgSO4 (10g/l), losartan, MgSO4 (3g/l) plus losartan, MgSO4 (10g/l) plus losartan, respectively. The animals received MgSO4 via drinking water for 9 days. In addition, losartan (10mg/kg/day; i. p.) was accompanied with MgSO4 from day 3. Groups 7-12 followed the same regimen of above groups, but CP (2.5mg/kg/day; i. p.) was added to regimen from day 3. At the end of day 9, all animals were sacrificed and the serum levels of blood urea nitrogen (BUN) and creatinine (Cr) were measured. The kidneys were removed rapidly for histopathological study. The Coadministration of losartan and MgSO4 (3g/l) decreased serum Cr and BUN levels in CP treated animals. Also, that was partially attenuated the kidney tissue damage. It was concluded that combination of losartan and MgSO4 (3g/l) may ameliorate kidney function against CP-induced failure.
RESUMO
OBJECTIVE: The present study was designed to further investigate the effect of amitriptyline, a classical tricyclic antidepressant, on carrageenan-induced paw edema in rats. METHODS: First, amitriptyline was administered intraperitoneally (i.p.) at doses of 20, 40 and 80 mg kg-1, 30 min before subplantar injection of carrageenan. Second, amitriptyline was given intracerebroventriculary or intrathecally at doses of 25, 50 and 100 μg/rat, 30 min prior to carrageenan challenge. Third, the effect of adrenergic receptor antagonists such as propranolol (10 mg kg-1, i.p.), prazosin (4 mg kg-1, i.p.) and yohimbine (10 mg kg-1, i.p.) and an opioid receptor antagonist (naloxone, 4 mg kg-1, i.p.) on the anti-inflammatory effect of amitriptyline (40 mg kg-1, i.p.) was investigated. RESULTS: Our data confirm that intraperitoneally administered amitriptyline exhibits a marked anti-inflammatory effect on carrageenan-induced paw edema in rats 4 h postcarrageenan challenge (P < 0.001). Intracerebroventricular (i.c.v.) administration of amitriptyline also reduced the development of paw edema at 4 h postcarrageenan (P < 0.001), but intrathecal (i.t.) application of amitriptyline failed to alter the degree of paw swelling. Furthermore, the applied antagonists did not modify the anti-inflammatory effect of amitriptyline. CONCLUSION: These results support the view that amitriptyline has a considerable anti-inflammatory effect on carrageenan-induced paw edema in rats and suggest that at least a part of this property could be mediated through supraspinal sites. Moreover, it seems unlikely that the investigated adrenergic and opioid receptors have a significant role in this effect of amitriptyline.