ABSTRACT
To examine the effect of silymarin [SM], a mixture of flavonoids and polyphenols extracted from Silybum marianum, on mesenteric ischemia-reperfusion [I-R] injury in a rat model. Fifty rats were randomly divided into 5 groups [n = 10]. Group 1 was sham operated, while groups 2-5 were subjected to mesenteric I-R lasting 1 h. Group 2 received isotonic sodium chloride, group 3 received SM [100 mg/kg/day] for 7 days before I-R, group 4 received SM for 7 days after I-R, and group 5 received SM for 7 days both before and after I-R. The rats were sacrificed by exsanguination in groups 1-3 at the 24th hour and groups 4 and 5 were sacrificed on the 7th day of reperfusion. Blood and intestinal specimens were taken for biochemical and pathological evaluations. Serum superoxide dismutase [SOD] and heat shock protein 70 levels were significantly higher in group 2 [5.24 +/- 1.76 U/l and 261.4 +/- 16.8 ng/ml] compared to the sham group [2.08 +/- 1.76 U/l and 189.9 +/- 28.7 ng/ml] [p < 0.001 and p < 0.0001, respectively]. However, SOD activity and the extent and severity of the histopathological lesions were significantly less in groups 3 [3.11 +/- 1.18 U/l, 1.0 [range 0.0-2.0]], 4 [2.15 +/- 0.87 U/l, 1.0 [range 1.0-3.0]], and 5 [1.80 +/- 0.61 U/l, 0.5 [range 0.0-2.0]], treated with SM, than in group 2 [5.24 +/- 1.76 U/l, 2.0 [range 2.0-3.0]] [p = 0.002, p < 0.001, and p = 0.0001; p < 0.001, p = 0.007, and p = 0.0001, respectively]. Also, TNF- alpha levels were lower in the SM-supplemented groups compared to group 2. Serum thiobarbituric acid-reactive substance concentrations were low in the pre-/posttreatment groups treated with SM compared to group 2. No statistical difference was observed for protein carbonyls between the groups. Our findings suggest that SM therapy may attenuate the oxidative and intestinal damage induced by I-R injuries
Subject(s)
Animals, Laboratory , Reperfusion Injury/drug therapy , Mesentery , Rats, Sprague-Dawley , IleumABSTRACT
We evaluated the genotypes of the serotonin transporter gene (5-HTT) in patients with premature ejaculation (PE) to determine the role of genetic factors in the etiopathogenesis of PE and possibly to identify the patient subgroups. A total of 70 PE patients and 70 controls were included in this study. All men were heterosexual, had no other disorders and were either married or in a stable relationship. PE was defined as ejaculation that occurred within 1 min of vaginal intromission. Genomic DNA from patients and controls was analyzed using polymerase chain reaction, and allelic variations of the promoter region of the serotonin transporter gene (5-HTTLPR) were determined. The 5-HTTLPR (serotonin transporter promoter gene) genotypes in PE patients vs. controls were distributed as follows: L/L 16% vs. 17%, L/S 30% vs. 53% and S/S 54% vs. 28%. We examined the haplotype analysis for three polymorphisms of the 5-HTTLPR gene: LL, LS and SS. The appropriateness of the allele frequencies in the 5-HTTLPR gene was analyzed by the Hardy-Weinberg equilibrium using the chi2-test. The short (S) allele of the 5-HTTLPR gene was significantly more frequent in PE patients than in controls (P<0.05). We suggest that the 5-HTTLPR gene plays a role in the pathophysiology of all primary PE cases. Further studies are needed to evaluate the relationship between 5-HTTLPR gene polymorphism and patient subgroup (such as primary and secondary PE) responses to selective serotonin reuptake inhibitors as well as ethnic differences.