جستجوی مقالات مرتبط با کلیدواژه "سیمواستاتین" در نشریات گروه "پزشکی"

Cardiac ischemia is the major cause of morbidity and mortality which can be increased by Statins. This study aimed to increase the effectiveness of simvastatin in the form of niosomes.

In this study, 25 male Wistar rats were divided into 5 groups: control, ischemia (induced by closed LAD), ischemia receiving nano-niosomes, ischemia receiving simvastatin, and ischemia receiving simvastatin-loaded nano-niosomes. One month after the drug injection, RNA was extracted from the heart tissue of the studied groups, cDNA was synthesized, and a real-time PCR test was performed using specific primers. SPSS 21.0 software was used for statistical analysis. Analysis of variance was used to investigate the effect of the interventions, and Tukey's post hoc test was used to investigate a significant difference (P<0.05) between the control groups and other groups as well as between intervention groups.

Apoptosis and autophagy increased significantly in the ischemia group compared to the control group (P<0.05). In the simvastatin-loaded nano-niosomes group, compared to the simvastatin group, apoptosis and autophagy showed a significant decrease (P<0.05), and also in both simvastatin-loaded nano-niosomes and simvastatin group, compared to the control group, apoptosis and autophagy showed a significant decrease. (P<0.05).

Simvastatin is an effective drug in the recovery of cardiac ischemia, but the main problem in using simvastatin is its instability and degradability, and the use of its niosomes form solves this problem properly.

Simvastatin‑loaded nano‑niosomes is more effective in reducing heart ischemia damage compared to simvastatin.

Pain is divided into two main types, fast and slow. Pain receptors are composed of free nerve endings and use two separate pathways to transmit pain signals to the CNS. Sharp pain signals are produced by mechanical and thermal pain stimuli. These signals are transmitted to the spinal cord by peripheral nerves through Aδ fibers at a speed of 3-15 m/s. On the contrary, slow and chronic pain signals are mainly produced by chemical pain stimuli, but sometimes stable mechanical or thermal stimuli can also produce these signals. These signals are transmitted to the spinal cord by C-type fibers at a speed of 0.5 to 2 m/s (1).The mechanisms of neuropathic pain are not fully known, but the mechanisms proposed in the pathogenesis of this pain include the role of glial cells as supporting cells of the central nervous system, changes in sodium and potassium voltage-dependent channels, afferents adjacent to the neuron. It is damaged. Different neural pathways are affected differently. Therefore, identification of these pathways is important in determining the analgesic and medicinal mechanisms from physiological aspects. Although there are many studies in this field, one of the existing problems is the rate of recovery and return of nerve activity after injury. The results of researchers' research have brought relatively acceptable results, which were not without problems. In the present research, due to the high incidence of peripheral nerve injuries caused by blows and fractures in humans and animals, efforts will be made to find a drug or drug combination to accelerate the healing process of damaged nerves following experimental sciatic nerve injury in the rat animal model. Therefore, the present study will be conducted in order to investigate the analgesic effects of simvastatin and its neurophysiological interaction with the involved systems following experimental sciatic nerve ligation in rats.

This research was used in 2 experimental phases on 85 adult male rats weighing 180-200 grams. These animals were transferred to the laboratory animal breeding and maintenance center of the veterinary school and were kept in standard mouse cages under standard conditions. All animals were evaluated for motor health before surgery, and then all mice were anesthetized by intraperitoneal injection of ketamine hydrochloride (60 mg/kg) and xylazine (10 mg/kg), and after scrubbing and initial leg preparation The animals were placed on their left side and an incision was made in the posterior-external skin of the thigh area of ​​the left leg. The muscles and fascia were gently removed and after exposing the sciatic nerve, the sciatic nerve was compressed for 60 seconds using a micro hemostat. In order to trace, the injury site is marked by suturing the muscle closest to the crush site using non-absorbable silk suture (0-5) and then the muscles are placed together and the subcutaneous tissue and skin are The sequence was stitched using vicryl thread (0-4) and nylon (0-3) in a simple all round and single stitch method. Then formalin test was done and licking time was measured. The animals were divided into 4 groups: group 1: nerve damage without treatment, group 2, 3 and 4 were treated with simvastatin. Mice in group 2 (with a dose of 2 mg/kg), group 3 (with a dose of 4 mg/kg) and group 4 (with a dose of 8 mg/kg) were treated with Sivastatin. There were 5 mice in each group and they were evaluated in two time intervals of 2 and 4 weeks.

As seen in Figure 1, the injection of morphine (5 mg/kg) significantly reduced the pain time caused by the formalin test compared to the control group (P<0.05). The level of 4 and 8 mg/kg simvastatin significantly decreased the pain time caused by the formalin test compared to the control group (P<0.05).According to the results of the statistical analysis of repeated measurements of one factor, the summary of the analysis of variance of the changes in the duration of the animal's response to the stimulating effects of formalin affected by the effective dose (8 mg/kg) of simvastatin compared to naloxone during the acute and chronic phases is presented in Figure 2.Naloxone injection (2 mg/kg) had no effect on pain time caused by formalin test compared to the control group (P>0.05). The level of 8 mg/kg simvastatin significantly decreased the pain time caused by the formalin test compared to the control group (P<0.05). The combined injection of naloxone plus simvastatin significantly reduced the analgesic effects of simvastatin compared to the simvastatin alone group (P<0.05).According to the results of the statistical analysis of the repeated measurements of one factor, the summary of the analysis of variance of the changes in the duration of the animal's response to the stimulating effects of formalin affected by the effective dose (8 mg/kg) of simvastatin compared to speroheptadine during the acute and chronic phases is presented in Figure 3.According to the results of the statistical analysis of the repeated measurements of one factor, the summary of the analysis of variance of the changes in the duration of the animal's response to the stimulating effects of formalin affected by the effective dose (8 mg/kg) of simvastatin compared to cimetidine during the acute and chronic phases is presented in graph No. 4 .

The aim of this study is the analgesic effects of simvastatin following experimental sciatic nerve ligation in rats. According to the obtained results, it was determined that the analgesic effects of simvastatin are dose-dependent and the findings of this test show that the effective dose (8 mg/kg) of simvastatin alone has been able to create a significant effect in reducing the painful effects of formalin in animals. It has also caused a significant decrease in the response time to formalin pain stimulus in animals. Antagonists naloxone, cyproheptadine and cimetidine were able to inhibit the analgesic effects in acute and chronic phase. Simvastatin activates the PI3K/AKt pathway and increases neurogenesis through BDNF and (Vascular endothelial growth factor) (12). Simvastatin increases the phosphorylation and expression of BDNF and VEGF gene in (Dentate gyrus) DG. As a result, cell proliferation increases and differentiation occurs in the DG area and brain recovery increases (14). Therefore, simvastatin may cause gene expression of growth factors, production of protein kinases, and subsequent induction of neurogenesis in the DG of the hippocampus, increasing dendritic branches through the activation of AKt through the signaling pathway (15). The effects of simvastatin on ischemia-reperfusion injury of the sciatic nerve in adult rats, as a result, administration of simvastatin before ischemia shows protective properties in nerve re-injury and improves blood supply again (16).

Exposure to ethanol as a neurotratogen in the developmental period has destructive effects on the central nervous system and causes neurological disorders in adulthood. These disorders are associated with apoptosis in areas of the brain such as the hippocampus, by activating the oxidative-inflammatory cascade and high levels of nerve degeneration. Simvastatin, used as a drug to treat hypercholesterolemia, can cross the blood-brain barrier and its neuroprotective effects have been confirmed in several diseases of the nervous system. This study aimed to evaluate the protective activities of simvastatin on memory disorders and nerve cell necrosis in the rat hippocampus by postnatal alcohol exposure.

Male rat infants received 5.27 g / kg milk powder soluble ethanol on days 2-10 after birth by gavage. They also received 10 and 20 mg/kg of simvastatin on days 2-10 after birth subcutaneously. Cognitive memory abnormalities were assessed 36 days after birth by the new object detection and then, the number of necrotic cells was assessed by nissl staining.

Behavioral data showed that in the groups treated with simvastatin, the new object recognition memory increased compared to the ethanol group (P<0.01). In addition, in the ethanol group, an increase in cell death was observed in the CA1 region of the hippocampus, and treatment with simvastatin showed a significant decrease in the number of necrotic cells (P<0.01).

This study showed that simvastatin has a protective effect on alcohol-related neurological defects, although more research is needed in the future.

Venlafaxine is an antidepressant that belongs to the family of selective serotonin and norepinephrine reuptake inhibitor (SNRIs) drugs. Recent studies have indicated that prolonged use of antidepressants leads to a state where increased formation of reactive oxygen species (ROS) overwhelms body antioxidant protection and subsequently induces DNA damage, lipid peroxidation, protein modification and cytotoxicity. This study attempts to examine the protective effect of simvastatin against venlafaxine induced cytotoxicity and oxidative stress in human gingival fibroblasts (HGF) cells.

In this experimental study, the intracellular ROS generation and IC50 were measured in cells treated with venlafaxine and simvastatin at different concentrations (50, 100, 150, and 200 μM) in pre-treatment in vitro condition.

According to findings, HGF cell viability was significantly different in 150, and 200 μM of simvastatin compared with venlafaxine (P<0.01). Also, simvastatin significantly decreased the effects of venlafaxine by reducing the level of ROS at 150 and 200 μM (P<0.01).

This study suggests that simvastatin attenuates venlafaxine-induced cytotoxicity in HGF cells through scavenging excessive ROS.

Today, implant treatment is one of the most popular dental treatments. To have a successful long-lasting implant treatment, enough bone is needed in that area. Given the positive effects of simvastatin on osteogenesis, this research aimed to compare the effect of freeze-dried bone allograft with and without simvastatin in extracted tooth socket in rats.

This experimental study was conducted in 72 Wistar rats (300 gr). Then rats were randomly divided into two groups (control and intervention). We evaluated osteogenesis, inflammation and granulation tissue formation after four and eight weeks. Data analysis was done applying ANOVA and Tukey post-test in SPSS V22.

After four and eight weeks, there were significant differences in the rate of osteogenesis between the intervention groups (FDBA+Simvastatin and FDBA) (P= 0.001). A thsese times, the rates of inflammation were found to be significantly lower in animals that received FDBA+Simvastatin compared to the control group (P<0.001). At weeks four and eight, the amount of granulation tissue was lower in FDBA+Simvastatin group than the FDBA group (P<0.05).

The study showed that simvastatin can significantly increase the amount of osteogenesis and also could reduce inflammation and granulation tissue formation.

Cancer is a disharmony amongst cell growth and death which results in accumulation of cells. Bone cancer is an absolutely dangerous type of cancer and occurs when the bone-making cells are disrupted. Despite some reports on the anticancer effects of simvastatin, the activity of simvastatin on bone cancer cells has not been reported. The aim of this study was to evaluate the cytotoxic and apoptotic effects of simvastatin on bone cancer MG63 cell line.

In this study, the MG63 cells were cultured and then the cells were incubated with different concentrations of simvastatin for 24 h and the IC50 dose was measured using MTT test. The effects of simvastatin on the mechanisms of cell death such as apoptosis and necrosis were evaluated by flow cytometry. Real-time PCR was used to evaluate the gene expression of caspase 3, 8 and 9 enzymes and Finally, cells treated with IC50 dose of simvastatin were examined by Hoechst staining technique. The collected data were analyzed using the student’s T statistical test and then SPSS software.

The MTT results showed that simvastatin at a dose of 155 µg/Ml destroys 50 % of cancer cells. On the other hand, flow cytometry analysis showed that MG63 cells treated with simvastatin (300 µg/Ml) had apoptotic cell death over 90 % compared to the control group. Evaluation of caspase 3, 8 and 9 enzymes using real-time PCR indicated that there was a significant difference in caspase 3 and 9 gene expression (p<0.001) but, no significant difference was observed in caspase 8 gene expression (p<0.05). In the Hoechst staining technique, the discoloration of the treated group cells compared to the control group indicated that the cell nucleus was densified and disintegrated, indicating apoptotic cell death.

Finally, the results of this study showed that simvastatin in cell culture medium can induce cytotoxic and apoptotic effects in bone cancer cells (MG63 cell line), therefore, it is important to consider the possibility of using simvastatin in the treatment of bone cancer.

Contrast-induced nephropathy (CIN) is a serious complication following contrast-based imaging methods, e.g. receiving iodixanol. Statins have been postulated to prevent CIN via various mechanisms. However, there have been conflicting reports on the use of statins for prevention of CIN. The aim of this study was to assess the effectiveness of simvastatin in the prevention of CIN.

A total number of 194 patients were randomly allocated to groups of control and statin-treated patients (n = 97 in both groups). The two groups received the same dose of iodixanol. The control group received normal saline before and after angiography and statin-treated patients received simvastatin (80 mg/day) and normal saline before and after angiography. Serum creatinine levels were measured before angiography and two consecutive days after the procedure. Glomerular filtration rate (GFR) was calculated on the second and third days. The values were then statistically analyzed.

There were no differences between the two groups in the first 24 hours after the procedure. However, after 48 hours, GFR values were significantly higher in the statin-treated group (P = 0.002).

Prophylactic administration of statins along with hydration may be associated with less contrast-induced nephropathy.

Various therapeutic protocols have been recommended for treating dyslipidemia، particularly in patients with coronary artery disease. The purpose of this study was to assess the efficacy of statin use with or without fenofibrate on echocardiographic findings of patients with coronary artery disease and dyslipidemia.

This clinical trial was conducted on 124 patients with coronary artery disease and dyslipidemia in Baqiyatallah Hospital in Tehran، Iran during 2008 to 2010. The first group of patients (64) received simvastatin (20 mg) and fenofibrate (200 mg) with low lipid diet and exercise while the second group (60) only received simvastatin with low lipid diet and exercise for one year.

The mean age of the participants was 54. 3±6. 5 years. The first group showed significant changes in lipid profile and left ventricular ejection fraction (LVEF)، (P<0. 05). Left ventricular diastolic function parameters showed no significant changes in both groups upon 12 months of treatment.

The results of this study show، one-year treatment by simvastatin and fenofibrate can be effective on lipid profiles، and improve LVEF with resultant positive effect on heart function.