Effects of statins on experimental colitis in normocholesterolemic rats

Objective. The results of previous studies suggest that statins have a direct anti-inflammatory effect that is not directly related to their cholesterol-lowering activity. The aim of this study was to investigate the effect of simvastatin (SIM) and fluvastatin (FLU) on trinitrobenzene sulfonic acid (TNBS)-induced colonic inflammation in rats. Material and methods. The drugs were given for 3 days (0.1 and 1 mg/kg day^?1; intraperitoneally) after induction of colitis. The lesions in the distal colon were scored at the macroscopic and microscopic level. Tissue malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were assessed and formation of reactive oxygen species and peroxynitrite was monitored by chemiluminescence (CL) assay. Trunk blood was collected for the measurement of serum tumor necrosis factor (TNF)-α level. Results.Treatment with SIM reduced the lesion score of the colitis group at macroscopic level (p<0.05), but there was no effect of treatment with FLU. The increase in colonic MDA level of the colitis group was reduced by both drugs at all doses (p<0.05–0.001). The decrease in GSH and the an increase in MPO activity in the colitis group were reversed by SIM at all doses (p<0.01), but FLU had no effect. An increase in colonic lucigenin CL value in the colitis group was reduced by SIM and FLU at all doses (p<0.001) and an increase in peroxynitrite ratio in the colitis group showed a significant reduction in SIM-treated groups; FLU reduced this effect at a dose of 1 mg/kg (p<0.01). An increase in tissue collagen content and serum TNF-α level in the colitis group was reversed by both drugs at all doses (p<0.001). Conclusions. SIM and FLU seemed to be beneficial in a TNBS-induced rat colitis model through the prevention of lipid peroxidation, superoxide generation, cytokine production and neutrophil accumulation.     

The beneficial effect of resveratrol on rat bladder contractility and oxidant damage following ischemia/reperfusion

OBJECTIVE: The present study aimed to investigate the possible beneficial activities of resveratrol (3,5,4'-trans-trihydroxystilbene), a natural phytoalexin, on contractility and oxidant damage after ischemia/reperfusion (I/R) of the rat urinary bladder. MATERIALS AND METHODS: The abdominal aorta of Sprague-Dawley rats was occluded for 60 min to induce ischemia and then allowed 60 min of reperfusion. Resveratrol (10 mg/kg) or saline was administered intraperitoneally 15 min before ischemia and immediately before reperfusion. In the sham-operated group, the abdominal aorta was left intact and the animals were treated with resveratrol or saline. The bladder samples were either used for functional studies or stored for biochemical assays. RESULTS: In the I/R group, the isometric contractile responses of the bladder strips to carbachol (CCh; 10(-8)-10(-4) mol/l) were lower than those of the control group and were reversed by treatment with resveratrol. Histological evaluation revealed loss of urothelial cells, detachment and loss of urothelial cells and local ulcerated areas and severe inflammatory cell infiltration in the untreated I/R group, and regeneration of luminal mucosa and a significant decrease in the density of the inflammatory cell population in the resveratrol-treated I/R group. Lipid peroxidation and the myeloperoxidase activity of the bladder tissues in the I/R group were higher than in the sham-operated group. Resveratrol treatment in the I/R group decreased these parameters compared with I/R alone. Similarly, the significant decrease in tissue glutathione level in the I/R group compared with controls was also prevented by resveratrol. Conclusion: Treatment with resveratrol almost completely reversed the low contractile responses of the rat urinary bladder to CCh and prevented oxidative tissue damage following I/R.     

Propylthiouracil (PTU)-induced hypothyroidism alleviates burn-induced multiple organ injury

Oxidative stress has an important role in the development of multiorgan failure after major burn. This study was designed to determine the possible protective effect of experimental hypothyroidism in hepatic and gastrointestinal injury induced by thermal trauma. Sprague Dawley rats were administered saline or PTU (10 mgkg(-1) i.p.) for 15 days, and hypothyroidism was confirmed by depressed serum T(3) and T(4) concentrations. Under brief ether anesthesia, shaved dorsum of rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10s. PTU or saline treatment was repeated at the 12th hour of the burn. Rats were decapitated 24h after injury and tissue samples from liver, stomach and ileum were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Tissues were also examined microscopically. Tumor necrosis factor (TNF)-alpha and lactate dehydrogenase (LDH) were assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity, CL levels and collagen content of the studied tissues (p<0.05-0.001). Similarly, serum TNF-alpha and LDH were elevated in the burn group as compared to control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by thermal trauma. Our results suggest that PTU-induced hypothyroidism reduces oxidative damage in the hepatic, gastric and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.     

Ectopic thyroid in the abdomen: Report of a case

Ectopic thyroid tissue can be seen anywhere along the path of the descending glands, but it is rarely seen in the abdominal cavity. An ectopic thyroid was encountered incidentally in the pancreas of a 50-year-old woman who underwent a bilateral truncal vagotomy and pyloroplasty for a duodenal ulcer. There were no signs or symptoms of a thyroid tumor.     

Caffeic acid phenethyl ester (CAPE) prevents methotrexate-induced hepatorenal oxidative injury in rats

Objectives This study aimed to investigate the antioxidant and anti‐inflammatory effects of caffeic acid phenethyl ester (CAPE) on the methotrexate (MTX)‐induced hepatorenal oxidative damage in rats. Methods Following a single dose of methotrexate (20 mg/kg), either vehicle (MTX group) or CAPE (10 µmol/kg, MTX + CAPE group) was administered for five days. In other rats, vehicle (control group) or CAPE was injected for five days, following a single dose of saline injection. After decapitation of the rats, trunk blood was obtained, and the liver and kidney tissues were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and sodium potassium‐adenosine triphosphatase (Na⁺/K⁺‐ATPase) activity. TNF‐α and IL‐1β levels were measured in the blood. Key findings Methotrexate administration increased the tissue MDA levels, MPO activity and decreased GSH levels and Na⁺/K⁺‐ATPase activity, while these alterations were reversed in the CAPE‐treated MTX group. Elevated TNF‐α and IL‐1β levels were also reduced with CAPE treatment. Conclusions The results of this study revealed that CAPE, through its anti‐inflammatory and antioxidant actions, alleviates methotrexate‐induced oxidative damage, which suggests that CAPE may be of therapeutic benefit when used with methotrexate.     

Radiolabeling of EGCG with <Superscript>131</Superscript>I and biodistribution in rats

Epigallocatechin gallate (EGCG), is the most abundant and widely studied catechin in green tea (Camellia sinensis Theaceae). The inhibitory effects of EGCG and green tea extract on carcinogenesis in various organs in rodents have now been demonstrated over the past decade. The aim of study was to label EGCG with I-131, to determinate its structure and to evaluate its biodistribution in Wistar rats. Radiolabeling was carried out by direct electrophilic iodination method (iodogen) and yield was determined by radio thin layer chromatography (RTLC). Radiolabelling yield is determined as 89 ± 1.0%. Besides, determination of structure of iodinated molecule, serum stability, and partition coefficient experiments was performed. The structure analysis of synthesized cold ¹²⁷I-EGCG complex was assessed with LC–MS–MS and ¹H-NMR. ¹H-NMR and LC–MS–MS results of iodinated EGCG (¹²⁷I-EGCG) show that oxidize iodine reacts electrophilic with aromatic ring. Serum stability results showed that in vitro stability of ¹³¹I-EGCG was quite high. It is observed that labeling percentage decreased 83 ± 2% at 24th, Partition coefficient results show that the partition coefficient of EGCG was calculated as theoretical partition coefficient = 2.04 ± 0.42 and the experimental partition coefficient of ¹³¹I-EGCG was found as 1.46 ± 0.2. The biodistribution data shown that the maximum uptake of the radioiodinated EGCG was seen in lung and pancreas at 30 min. The blocking assay results indicated that the uptake of ¹³¹I-EGCG in lung was not significantly change (0.25, 0.23, and 0.22%ID/g at 30, 60, and 150 min, respectively). Biodistribution data showed no significant uptake in a specific organ of the rat. Hence radiolabeled EGCG is seen in some organs (lung, liver, pancreas, kidney, etc.).     

A patient with established primary progressive multiple sclerosis transitions to 'secondary' relapsing-remitting disease course following a fulminant demyelinating episode

Primary progressive multiple sclerosis (PPMS), relapsing remitting MS (RRMS) and acute disseminated encephalomyelitis (ADEM) are clinically and immunopathogenetically distinct phenotypes of inflammatory demyelinating disorders of the central nervous system. Progression following RRMS is well described as secondary progressive MS. We report a patient with unexpected transition from long established PPMS to clinically and radiologically active RRMS after an ADEM-like fulminant demyelinating episode despite an immunosuppressive treatment preceding relapses. We note clearly accelerated brain atrophy after the RRMS course ensues. The unique disease course in this patient illustrates the dissociation of the biology and disability impact of relapses and progression.     

Microcomputed tomographic analysis of bone microarchitecture after sinus augmentation with hyaluronic matrix: a case–control study

Background

The aim of this study was to analyze trabecular microarchitecture of augmented sinuses with hyaluronic matrix and xenograft by microcomputed tomography, and to investigate whether hyaluronic matrix has an effect on the newly formed bone quality.

Materials and methods

Thirteen patients undergoing maxillary sinus augmentation were included in this split-mouth study. Right and left sinus sites were randomly assigned to test and control group. In test group, the sinus was grafted with hyaluronic matrix and xenograft; in control group, only with xenograft. Four months after augmentation, bone samples were harvested during implant placement and analyzed for the following trabecular microarchitecture parameters using microcomputed tomography: bone volume (BV), total volume (TV), bone volume fraction (BV/TV), bone surface (BS), specific bone surface (BS/BV), bone surface density (BS/TV), trabecular thickness (Tb.Th), trabecular separation (Tb.Sp), trabecular pattern factor (Tb.Pf), and fractal dimension (FD).

Results

There was statistically significant difference only for BS/TV parameter between two groups. BS/TV was higher in hyaluronic matrix group compared with control group.

Conclusions

Addition of hyaluronic matrix to xenograft may enhance bone quality in terms of bone surface density. However, more research investigating the microstructural variation of augmented sinuses is needed with a greater sample.