Carvacrol is the major compound of essential oils of many plants, ethnomedically used for centuries but there were no detailed investigations on its action on the cardiovascular system. The aim of our study was to investigate the role of carvacrol on the cardiovascular functions of anesthetized rats and in vitro of isolated rat aorta. Carvacrol (100 microg/kg, I. P.) decreased heart rate, mean arterial pressure and systolic and diastolic blood pressures of the anesthetized rats whereas there were no effects at 1, 10 and 20 microg/kg. Carvacrol was observed to exhibit hypotension and to inhibit N((omega))-nitro- L-arginine methyl ester ( L-NAME)-induced hypertension. The lack of inhibitory action of carvacrol (10 (-4) M) on the CaCl (2)- and phenylephrine-induced contractions of isolated rat aorta showed that neither adrenergic receptors nor voltage-dependent vascular L-type calcium channels were involved. But, based on previous investigations, the involvement of cardiac L-type calcium channel blocking actions are suggested for the hypotensive actions of carvacrol was assumed.

Tumor necrosis factor-alpha (TNF-alpha) has been established as an important mediator in renal ischemia-reperfusion (I/R) injury. Leptin, a product of the ob gene, has been known to exhibit cytoprotective effects on renal tissue, but its effect on renal tissue TNF-alpha level after renal I/R injury in rats remains unknown. The purpose of the study was to evaluate the effects of leptin on renal tissue TNF-alpha, malondialdehyde (MDA), protein carbonyls (PCs) and total sulfydryl group (SH) levels, and plasma nitrite levels after renal I/R injury in rats. The animals were divided into three groups: control, I/R and I/R+leptin. Rats were subjected to renal ischemia by clamping the left pedicle for 45 min, and then reperfused for 1 h. The I/R+leptin group was pretreated intraperitoneally with leptin (10 microg/kg) 30 min before the induction of ischemia. Our results indicate that MDA, TNF-alpha levels, and PCs were significantly higher in the I/R group than those in the control group (p < 0.05). The administration of leptin decreased these parameters (p < 0.05) significantly. The SH level was observed to significantly decrease after I/R injury when compared to the control group (p < 0.05). Leptin treatment significantly increased tissue SH and plasma nitrite levels when compared to the I/R group (p < 0.05). Plasma nitrite levels did not change significantly in I/R when compared to the control. These results suggest that leptin could exert a protective effect on I/R induced renal damage by decreasing TNF-alpha levels and increasing nitrite level.

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The objective of the present study was to investigate the effect of leptin on the progression of colorectal carcinoma to metastatic disease by analyzing the serum leptin concentration and Ob-R gene expression in colon cancer tissues. Tissue samples were obtained from 31 patients who underwent surgical resection for colon (18 cases) and metastatic colon (13 cases) cancer. Serum leptin concentration was determined by an enzyme-linked immunosorbent assay (ELISA) and Ob-R mRNA expression by real-time polymerase chain reaction (RT-PCR) for both groups. ELISA data were analyzed by the Student t-test and RT-PCR data were analyzed by the Mann-Whitney U-test. RT-PCR results demonstrated that mRNA expression of Ob-R in human metastatic colorectal cancer was higher than in local colorectal cancer tissues. On the other hand, mean serum leptin concentration was significantly higher in local colorectal cancer patients compared to patients with metastatic colorectal cancer. The results of the present study suggest a role for leptin in the progression of colon cancer to metastatic disease without weight loss. In other words, significantly increased Ob-R mRNA expression and decreased serum leptin concentration in patients with metastatic colon cancer indicate that sensitization to leptin activity may be a major indicator of metastasis to the colon tissue and the determination of leptin concentration and leptin gene expression may be used to aid the diagnosis.

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We investigated the effect of thiamine (B1) treatment on bladder dysfunction in streptozotocin (STZ)-induced diabetic rats. A total of 40 rats were randomly divided into four groups: a control group, a group given thiamine only, a diabetic group and a diabetic group given thiamine therapy. Diabetes was induced in the rats by 65 mg/kg STZ via an intraperitoneal injection. Thiamine was given 50 mg/kg/day. Diabetic cystopathy was confirmed on cystometry 8 weeks later in diabetic groups. Rats' body and bladder weights were measured. Contractile response to carbachol and potassium chloride (KCl) of detrusor strips in all groups was studied in vitro. The body weights were significantly decreased (p<0.01), the bladder weights were significantly increased (p<0.01), and the cystometric bladder capacity and the residual urine volumes were significantly increased (p<0.001, p<0.01 respectively) in STZ-induced diabetic groups compared to the control group and the group given thiamine only. Contractile responses increased in the diabetic group in high carbachol and KCl concentrations (p<0.01, p<0.01, respectively). On the other hand, there were no differences in the other groups. These data suggest that high-dose thiamine (B(1)) treatment may be beneficial in delaying the progression of diabetic cystopathy in this experimental animal model.