Is there a new pathway relationship between melatonin and FEZ1 in experimental rat model of Alzheimer's disease?

Alzheimer's disease (AD) is a progressive neurodegenerative disease. This study was performed to determine the possible relationship between melatonin, which is known to play a role in the neuro-protective mechanism in AD, and fasciculation and elongation protein zeta 1 (FEZ1). Thirty male rats were included and separated into 3 groups (n = 10) as vehicle (artificial cerebrospinal fluid), streptozotocin (STZ) and STZ+melatonin (MLT). Two intracerebroventricular (icv) injections of 3 mg/kg STZ were made 48 hours apart. MLT injections were implemented for 14 days (ip; 10mg/kg/day). The Morris Water Maze (MWM) test was performed and rats were sacrificed to assess FEZ1 gene expression and protein levels from the hippocampus tissues and serum levels of noradrenaline (NA), dopamine and serotonin were determined from the blood samples. It was determined that the FEZ1/ß-actin protein ratio in the STZ group was significantly higher than that of the Vehicle group (p < 0.05) and in the MLT­administered group, the protein levels were decreased to the levels observed in the Vehicle group. Serum NA levels of STZ and STZ+MLT groups were found to be lower than those in the Vehicle group, while no difference was found regarding dopamine and serotonin levels. These findings show that reversal of increased FEZ1 levels in AD-induced rats with melatonin administration is the evidence of the effect of melatonin through FEZ1 in AD (Tab. 2, Fig. 5, Ref. 67). Keywords: FEZ1, Alzheimer's disease, melatonin, rat, microtubules, mitochondria.

Protective effects of salusin-α and salusin-ß on renal ischemia/reperfusion damage and their levels in ischemic acute renal failure.

Salusin-α and salusin-ß are expressed in many tissues including the central nervous system, vessels and kidneys; they have been shown to decrease endoplasmic reticulum stress during heart ischemia/reperfusion (I/R) and to decrease apoptosis. We investigated the relation of salusin-α and salusin-ß levels to acute ischemic renal failure. We also investigated whether these peptides are protective against renal I/R damage. Fifty-three rats were divided into six groups: control, I/R, I/R + salusin-α1, I/R + salusin-α10, I/R + salusin-ß1 and I/R + salusin-ß10. After removing the right kidney, the left kidney was subjected to ischemia for 1 h and reperfusion for 23 h. The treatment groups were injected subcutaneously at the beginning of ischemia with 1 or 10 µg/kg salusin-α, and 1 or 10 µg/kg salusin-ß. Histopathology was assessed at the end of the experiment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) activity and malondialdehyde (MDA) levels were measured in the kidney tissue. Serum levels of blood urea nitrogen (BUN), creatinine (Cre), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1 beta (IL-1ß) also were measured. Levels of salusin-α and salusin-ß were measured in the serum and kidney tissues of the control and I/R groups. SOD, CAT and GSH-PX activities were decreased and the levels of MDA, TNF-α, IL-6, IL-1ß, BUN and Cre were increased in the I/R group compared to controls. Severe glomerular and tubular damage was apparent in the I/R group compared to controls. The level of salusin-ß was decreased in the serum and kidney tissue of the I/R group compared to controls, whereas the level of salusin-α was decreased in the serum and increased in the kidney tissue. Salusin-α and salusin-ß administration increased SOD and GSH-PX enzyme activation and decreased the levels of MDA, TNF-α, IL-6 and IL-1ß compared to the I/R group. BUN and Cre levels were decreased in the I/R + salusin-α1 group and the level of Cre was decreased in I/R + salusin-ß10 group compared to the I/R group. We demonstrated a protective effect of salusin-α and salusin-ß against renal I/R damage. Changes in the levels of salusin-α and salusin-ß in the I/R group suggest that these peptides may be associated with acute renal failure.

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury.

The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were significantly increased compared with the control group. Significant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE significantly reduced these values. STZ-induced histopathological alterations including inflammatory cell infiltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic figure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondrial elongation were observed in cytoplasm of hepatocytes. CAPE significantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver.

Comparison of the effects of argon and neodymium:YAG laser iridotomy on cytokines in the rabbit aqueous humor.

PURPOSE: We compared the effects in rabbits of iridotomy using the argon or Nd:YAG laser on cytokines such as interleukin 1-beta (IL-1beta), interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha). METHODS: Twenty pigmented rabbits (20 eyes) underwent argon and Nd:YAG iridotomy under general and topical anesthesia. Group 1 (10 right eyes) was treated with the argon laser and group 2 (10 right eyes) with the Nd:YAG laser, using an equal number of shots and the same laser parameters for each group. Left eyes in both groups were evaluated as controls. Aqueous humor specimens were collected from each eye preoperatively and 1 and 3 days postoperatively. RESULTS: Aqueous IL-6 and TNF-alpha levels rose more on day 1 in the Nd:YAG group than the argon group. IL-6 and TNF-alpha levels were significantly higher on days 1 and 3 than the pre-operative and control levels (p<0.05). TNF-alpha levels on day 1 were significantly lower in the Nd:YAG than the argon group. There were no significant differences between the two laser groups for IL-6 on days 1 and 3. IL-1beta and IL-8 did not change CONCLUSIONS: Our findings suggest that cytokines, particularly IL-6 and TNF-alpha, may be inflammatory mediators in the early inflammation following argon and Nd:YAG laser iridotomies. These results also indicate that cytokines contribute to the acute effects of Nd:YAG and argon laser applications on inflammation.