Resistin Gene Promoter -420C>G (rs1862513) and +299 G>A (rs3745367) Polymorphisms in Psoriasis.

BACKGROUND: The pro-inflammatory adipokine resistin is known to be related to obesity, insulin resistance, and inflammation. Resistin's significance in the etiology of inflammatory illnesses, such as psoriasis, is explored herein. We examined the link between resistin gene polymorphisms (-420 C>G and +299 G>A) and psoriasis in the Turkish population. METHODS: In this study, we examined 107 patients with psoriasis and 103 healthy controls. Resistin -420 C>G (rs1862513) and +299 G>A (rs3745367) gene polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: In patients with psoriasis, the frequency of the resistin -420 CG genotype was meaningfully lower than in the controls. In comparison with the controls, the resistin +299 GA genotype and A allele frequencies were significantly higher. The Resistin -420 CG genotype significantly reduced the risk of psoriasis incidence, while the resistin +299 GA genotype and A allele were found to be associated with a higher risk of psoriasis. CONCLUSIONS: In the Turkish community, resistin gene polymorphisms at -420 C>G and +299 G>A may exert an important influence on psoriasis etiology and susceptibility.

MTHFR 677 C > T Gene Polymorphism is Associated with Large for Gestational Age Infants.

BACKGROUND: The aim of this study was to investigate the methylenetetrahydrofolate reductase (MTHFR) 677 C > T gene polymorphism in term infants born small (SGA), appropriate (AGA), and large for gestational age (LGA). METHODS: The study comprised 165 newborns with SGA, LGA and AGA. Genomic DNA was isolated from the peripheral blood. Samples were genotyped for MTHFR 677 C > T gene polymorphisms using PCR-RFLP. RESULTS: There was a statistically significant difference between the genotype and their allelic distribution of AGA, SGA, and LGA. The newborns carrying the TT genotype had higher birth weight than those carrying the CC and CT genotypes. The frequency of MTHFR 677 TT genotype and T allele was significantly higher and was found to be linked with a higher risk in LGA than in the AGA group. CONCLUSIONS: The MTHFR 677 C > T gene polymorphism can be used as a genetic marker in Turkish LGA newborns, but not in SGA.

Evaluation of the relationship between neonatal serum asprosin levels and anthropometric measurements in newborns of mothers with and without gestational diabetes mellitus.

BACKGROUND: Asprosin is a newly identified adipokine that is expressed in the placenta. Its production is increased in women with gestational diabetes mellitus (GDM), and it is a factor related to insulin resistance. This study aimed to determine whether neonatal serum asprosin levels are associated with anthropometric characteristics of newborns born to mothers with and without GDM. METHODS: This study included 51 newborns of mothers with GDM (insulin-treated or diet-treated) and 55 control newborns with their mothers. In newborns, anthropometric parameters were measured, and the concentrations of asprosin were detected by ELISA. Maternal blood glucose levels, body weight, and length were measured and body mass index (BMI) was calculated. RESULTS: Serum asprosin levels were significantly higher and linked to a higher risk in the newborns of mothers with GDM compared with those of the control newborns (170.3 [132.6] vs. 91.4 [68.7] ng/mL, p < 0.001). Serum asprosin levels were negatively correlated with blood glucose concentrations (r = -0.282, p = 0.045) in the newborns of mothers with GDM and significantly positively correlated with birth weight (r = 0.315, p = 0.019) in the control newborns. Newborn serum asprosin levels were positively correlated with the glucose levels (r = 0.264, p = 0.006) of all mothers. In addition, newborns born to an insulin-treated mother with GDM had significantly higher birth weight and length than newborns born to a diet-treated mother with GDM (3262.9 vs. 3137 g, p = 0.032, and 49.7 vs. 49.2 cm, p = 0.05). Although asprosin levels were higher in newborns of mothers treated with insulin, these differences were not statistically significant. Mothers with GDM had high blood glucose levels (p = 0.032). CONCLUSIONS: Serum levels of asprosin are increased and negatively correlated with glucose concentrations in newborns of mothers with GDM. Asprosin could be used as an early biomarker in newborns of GDM mothers.

Serum adiponectin levels and adiponectin +276 G/T gene polymorphism in newborns with large and small birth weights.

PURPOSE: Adiponectin may be an important indicator in the regulation of fetal and neonatal growth due to its metabolism, energy balance, and insulin-sensitizing action. The current study's goal was to determine if there is a link between adiponectin +276 G/T gene polymorphism and serum adiponectin level in newborns classified as appropriate for gestational age (AGA), small for gestational age (SGA), or large for gestational age (LGA). METHODS: The study included newborns classified as AGA (n = 65), SGA (n = 65), or LGA (n = 65) according to their gestational age or birth weight. To determine the presence of adiponectin +276 G/T gene polymorphism, genotyping was done using polymerase chain reaction-restriction fragment length polymorphism. Enzyme-linked immunosorbent assay was used to determine the level of adiponectin in the blood. RESULTS: The SGA newborns had significantly lower levels of serum adiponectin than the AGA and LGA newborns. There were statistically significant differences between the genotype frequencies (GG, GT, TT) of the SGA newborns (29.9%, 45.1%, 13.9%), the AGA newborns (41.6%, 20.7%, 44.4%), and the LGA newborns (28.6%, 34.1%, 41.7%) (chi-square = 15.8; degree of freedom = 4; p = .003). The newborns carrying the GT genotype had an increased risk of being SGA compared to those carrying the GG and TT genotypes (odds ratio [OR] = 3.07; confidence interval [CI] = 95% (1.38-6.64); p = .005 and OR = 6.96; CI = 95% (2.19-22.1); p < .001, respectively). The newborns carrying the GG and TT genotypes had better protection against being SGA than those carrying the GT genotype (OR = 0.33; CI = 95% (0.15-0.72); p = .005 and OR = 0.14; CI = 95% (0.05-0.46); p < .001, respectively). The newborns carrying the GT genotype had lower birth weights, head circumferences, and ponderal indices than those carrying the TT genotype (p < .001). The serum adiponectin levels between adiponectin +276 G/T genotypes did not differ significantly (p = .429). In addition, serum adiponectin level showed a significant positive correlation with birth weight, birth length, head circumference, and ponderal index in all newborns. CONCLUSION: The results of the current study suggest that the adiponectin +276 G/T gene polymorphism was associated with an increased chance of being born SGA or LGA. The effect of this polymorphism on newborn birth size was independently associated with serum adiponectin levels. Adiponectin may play a role in fetal growth.

TNF-α gene -238G>A polymorphism is associated with psoriasis patients.

BACKGROUND: Tumor necrosis factor-alpha (TNF-α) is a protein that plays a key role in the pathophysiology of chronic inflammatory disorders like psoriasis. AIMS: The goal of this study was to see whether the TNF-α gene -238G>A polymorphism was linked to psoriasis susceptibility. METHODS: This study comprised 90 psoriasis patients and ninety healthy controls. For the TNF-α gene -238G>A polymorphism, genomic DNA was extracted and genotyped using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) studies. RESULTS: Psoriasis patients had higher frequencies of the A allele and the AA genotype than the control group, and psoriasis was linked to the AA genotype (OR = 4.25, 95% CI = 1.37-13.1, p = 0.008) and the A allele (OR = 1.55, 95% CI = 1.01-2.34, p = 0.04). Patients with a family history of psoriasis showed an increase in the frequency of the AA genotype compared with GG and GA genotypes (46.7%, 36.7%, and 16.7%, p = 0.003, respectively). Furthermore, psoriasis patients with the AA genotype were discovered more commonly among those under 30 years of age and male patients than those with the GG and GA genotypes, but the differences were not statistically significant. CONCLUSION: The TNF-α gene -238G>A polymorphism has been related to an increased incidence of psoriasis.

Association between resistin gene (-420 C > G) polymorphism and acne vulgaris.

BACKGROUND: Acne vulgaris (AV) is the most prevalent inflammatory skin disease and develops on the face and upper trunk. Resistin, a member of the cysteine-rich secretory proteins family, is an adipokine expressed primarily in macrophages and monocytes; it has a role to play in the inflammatory period. AIMS: This study's purpose was to detect whether known resistin gene (-420 C > G) polymorphism plays a role in the pathogenesis of AV. METHODS: Patients with AV (n = 94) and healthy controls (n = 94) were enrolled in this investigation. Resistin gene (-420 C > G) polymorphism was decided by PCR-RFLP procedure. RESULTS: The distribution of genotype frequencies of resistin gene (-420 C > G) polymorphism was significantly different between the AV and healthy controls (p = 0.002). We found that the resistin gene (-420 C > G) CG genotype exhibited a significant association with decreased acne vulgaris risk. CONCLUSIONS: Our study is the first report investigating the relationship between the risk of AV and resistin gene (-420 C > G) polymorphism in the Turkish population. Resistin gene (-420 C > G) polymorphism is related to AV pathogenesis. CG genotype has a protective role and may be linked to a reduced risk of AV development. Furthermore, studies are needed to verify these findings in other populations.

Association of vaspin rs2236242 gene variants and circulating serum vaspin concentrations with coronary artery disease in a Turkish population.

Coronary artery disease (CAD) is the primary cause of death worldwide. Vaspin was a recently described adipokine, playing a protective role in many metabolic and cardiovascular diseases. This study aimed to assess the relation of serum vaspin levels and vaspin rs2236242 polymorphisms with CAD. The study included 105 healthy subjects and 105 CAD patients. Serum vaspin concentrations and vaspin rs2236242 polymorphisms were determined by enzyme-linked immunosorbent assay and polymerase chain reaction, respectively. There was a statistically significant difference between the genotypes of CAD patients (TT 26.7%, TA 71.4%, and AA 1.9%) and controls (TT 70.5%, TA 28.6%, and AA 1%; χ2 = 40.3; df = 2; p = .000). The TA genotype increased the risk of CAD (odds ratio [OR] = 6.60; 95% confidence interval [CI] = 3.60-12.1; p = .000) as compared to the TT genotype. There was a statistically significant difference between the allelic distribution of CAD patients (T 62.4% and A 37.6%) and controls (T 84.8% and A 15.2%; χ2 = 27.0; df = 1; p = .000). Those carrying the A allele had a higher risk of CAD compared to those with the T allele (OR = 3.35; 95% CI = 2.10-5.36; p = .000). The serum vaspin concentrations of the patients with TT, TA, and AA genotypes were 30.4 ± 1.72, 28.4 ± 2.89, and 36.4 ± 6.38 pg/ml, respectively, and there was no significant difference between the serum vaspin levels and vaspin genotypes (p = .696). All of the above suggested that the vaspin rs2236242 polymorphism was associated with CAD in the Turkish population.

Association between Vaspin rs2236242 Gene Polymorphism and Psoriasis Vulgaris.

BACKGROUND: Psoriasis known as a chronic inflammatory skin disease is accompanied by metabolic disorders such as obesity, diabetes, and dyslipidemia. Vaspin (a serine protease inhibitor derived from visceral adipose tissue) is a newly identified adipokine and a link between inflammation and obesity has been reported. We aimed to determine whether vaspin gene polymorphism is associated with the development and/or clinical features of psoriasis vulgaris. METHODS: Our study group consisted of 96 psoriasis vulgaris patients and 100 matched controls. Vaspin rs2236242 gene was genotyped using PCR. RESULTS: The vaspin genotypes showed a meaningful difference between psoriasis and control groups (p = 0.02). The frequency of the vaspin rs2236242 TT genotype was lower in psoriasis patients than in control participants (p < 0.05). The TA genotype was associated with a 2.38-fold increased risk of psoriasis compared to the TT genotype (p = 0.007, odds ratio: 2.38; 95% confidence interval: 1.25-4.55), but not the AA genotype. All subjects were the Turkish population, the study in other populations is needed and the sample size was small in number. CONCLUSION: Our study demonstrated that vaspin rs2236242 polymorphism is related to psoriasis in the Turkish population. Polymorphisms of the vaspin gene might serve as diagnostic biomarkers of psoriasis.

Chitotriosidase as a novel biomarker of early atherosclerosis in hemodialysis patients.

INTRODUCTION: Increasing evidence suggests that inflammation and increased macrophage activity have a central role in pathogenesis of atherosclerosis. It is shown that chitotriosidase (CHIT-1) is a marker of macrophage activity in atherosclerotic plaque, and is found associated with severity of atherosclerotic lesion. There is no data about CHIT-1 activity of hemodialysis patients in the literature. Thus, we hypothesized that in hemodialysis patients, CHIT-1 levels might be a novel biomarker in early atherosclerosis. METHODS: Forty-five hemodialysis patients were included in the study (age: 61.93 ± 13.34). Intima media thickness (IMT) was evaluated with high-resolution B-mode ultrasonography. Biomarker levels were measured in serum of patients. FINDINGS: We found positive correlation among IMT, age (R: 0.426, P: 0.004) and, CHIT-1 value (R: 0.462, P: 0.001) in spearman correlation analysis. When age, CRP, creatinine, P, Alb, CHIT-1 were chosen as measures that can effect IMT in multiple regression model, IMT level was related with CHIT-1 (Beta: 0,396, P: 0.012) and age (Beta: 0,313 P: 0,048) independently. DISCUSSION: In conclusion, this is the first report showing that serum CHIT-1 level was related independently with carotid IMT in hemodialysis patients. This biomarker might have an unknown role in the development of atherosclerosis during uremia.

Effects of ozone therapy on facial nerve regeneration.

INTRODUCTION: Ozone may promote moderate oxidative stress, which increases antioxidant endogenous systems. There are a number of antioxidants that have been investigated therapeutically for improving peripheral nerve regeneration. However, no previous studies have reported the effect of ozone therapy on facial nerve regeneration. OBJECTIVE: We aimed to evaluate the effect of ozone therapy on facial nerve regeneration. METHODS: Fourteen Wistar albino rats were randomly divided into two groups with experimental nerve crush injuries: a control group, which received saline treatment post-crush, and an experimental group, which received ozone treatment. All animals underwent surgery in which the left facial nerve was exposed and crushed. Treatment with saline or ozone began on the day of the nerve crush. Left facial nerve stimulation thresholds were measured before crush, immediately after crush, and after 30 days. After measuring nerve stimulation thresholds at 30 days post-injury, the crushed facial nerve was excised. All specimens were studied using light and electron microscopy. RESULTS: Post-crushing, the ozone-treated group had lower stimulation thresholds than the saline group. Although this did not achieve statistical significance, it is indicative of greater functional improvement in the ozone group. Significant differences were found in vascular congestion, macrovacuolization, and myelin thickness between the ozone and control groups. Significant differences were also found in axonal degeneration and myelin ultrastructure between the two groups. CONCLUSION: We found that ozone therapy exerted beneficial effect on the regeneration of crushed facial nerves in rats.

MicroRNA-125b as a new potential biomarker on diagnosis of renal ischemia-reperfusion injury.

BACKGROUND: Acute renal failure is commonly seen in the perioperative period. Ischemia-reperfusion (IR) injury plays a major role in acute renal failure and delayed graft function. MicroRNAs (miRs), which are pivotal modulators of cell activities, offer a major opportunity for affective diagnosis and treatment strategies because they are tissue specific and in the center of gene expression modulation. The effect of bardoxolone methyl (BM) on miR-21, miR-223-5p, and miR-125b in renal IR injury was evaluated in this study. METHODS: Wistar-Albino rats (12-16 wk old, weighing 300-350 g) were used in the study. Rats (n = 6) were randomized into three groups (control, IR, and BM + IR). Tissue levels of miRs were analyzed with reverse transcription polymerase chain reaction. RESULTS: Significant reduction of urea and total oxidant status, increase of total antioxidant status, and oxidative stress index were identified in the IR + BM group compared with the IR group. Significant increases of miR-21 (2842.82-fold) and miR-125b (536.8-fold) were identified in the IR group compared with the control group; however, miR-223-5p levels did not show any significant difference. Also, miR-21 and miR-125b were significantly reduced in the IR + BM group compared with the IR group. Reduced histopathologic changes were observed in the IR + BM group. A significant decrease in the number of tunel-positive cells was identified in the IR + BM group compared with the IR group. CONCLUSIONS: miR-125b was significantly increased in IR injury; thus, miR-125b can be a potential novel marker that can be used in diagnosis and treatment of renal IR injury. BM reduces miR-21 and miR-125b in case of IR injury and makes functional and histopathologic repairs.

Micro RNA-320 as a novel potential biomarker in renal ischemia reperfusion.

AIM: MicroRNAs (miR) are important diagnostic and treatment targets due to their different tissue expressions and their central position in the regulation of gene expressions. miR studies might pioneer emerging of new diagnostic tools and treatment goals in kidney diseases. Captopril (CAP) and telmisartan (TEL) were shown to be effective in ischemia reperfusion (IR) injury. There is not any study about the effect of TEL and CAP over miR-21-320-146a. Our aim was to study the effects of CAP and TEL over miR on renal IR model. METHODS: We used 12-16 weeks-old Wistar-Albino rats that weigh 300-350 g. Rats (n, 6) were randomized into four groups (Control, IR, IR + CAP, IR + TEL). Urea, creatinine, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), super oxide dismutase (SOD), and miRs were analyzed. RESULTS: Urea, creatinine, TOS, OSI levels of IR + CAP, and IR + TEL groups were lower comparing to IR group. TAS and SOD levels were higher in IR group than IR + TEL group. miR-21-320-146a showed increase in renal IR injury. miR-320, 146a showed significant decrease in IR + CAP and IR + TEL groups comparing to IR group. We showed histopathological recovery and decreased apoptosis in IR + CAP and IR + T groups than IR group. CONCLUSION: We, for the first time in the literature, showed that miR-320 is increased in IR injury. miR-320 might be a novel diagnosis and treatment target in renal ischemic reperfusion injury. Also, for the first time, we showed that CAP and TEL cause functional and histopathological recovery and lower miR-146a and miR-320.

Gastroprotective effects of sulforaphane and thymoquinone against acetylsalicylic acid-induced gastric ulcer in rats.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) commonly cause gastric ulcers (GUs). We investigated the effects of sulforaphane (SF) and thymoquinone (TQ) in rats with acetylsalicylic acid (ASA)-induced GUs. MATERIALS AND METHODS: Thirty-five male Wistar-Albino rats were divided into five groups: control; ASA; ASA with vehicle; ASA + SF; and ASA + TQ. Compounds were administered by oral gavage before GU induction. GUs were induced by intragastric administration of ASA. Four hours after GU induction, rats were killed and stomachs excised. Total oxidant status, total antioxidant status, total thiol, nitric oxide, asymmetric dimethylarginine, tumor necrosis factor-alpha levels, superoxide dismutase activity, and glutathione peroxidase activity in tissue were measured. Messenger RNA expression of dimethylarginine dimethylaminohydrolases, heme oxygenase-1 (HO-1), nuclear factor erythroid 2-related factor 2, and nuclear factor kappa-light-chain-enhancer of activated B cells were analyzed. Renal tissues were evaluated by histopathologic and immunohistochemical means. RESULTS: SF and TQ reduced GU indices, apoptosis, total oxidant status, asymmetric dimethylarginine, and tumor necrosis factor-alpha levels, nuclear factor kappa-light-chain-enhancer of activated B cells, and inducible nitric oxide synthase expressions (P < 0.001, P = 0.001). Both examined compounds increased superoxide dismutase activity, glutathione peroxidase activity, total antioxidant status, total thiol, nitric oxide levels, endothelial nitric oxide synthase, dimethylarginine dimethylaminohydrolases, HO-1, nuclear factor erythroid 2-related factor 2, and HO-1 expressions (P < 0.001). CONCLUSIONS: These results suggest that pretreatment with SF or TQ can reduce ASA-induced GUs via anti-inflammatory, antioxidant, and antiapoptotic effects. These compounds may be useful therapeutic strategies to prevent the gastrointestinal adverse effects that limit nonsteroidal anti-inflammatory drugs use.

Effect of ukrain on ischemia/reperfusion-induced kidney injury in rats.

BACKGROUND: The aim of this study was to investigate the potential protective effect of ukrain on an experimental kidney injury model induced by ischemia and reperfusion (IR) in rats. MATERIAL AND METHODS: A total of 24 male Sprague-Dawley rats were equally and randomly separated into three groups as follows: group-1: controls (C; only laparotomy); group 2: renal ischemia-reperfusion (IR; occlusion of the renal artery for 30 min and 2 h of reperfusion); and group 3: ukrain treatment and IR applied group (U + IR; occlusion of the renal artery for 30 min and 2 h of reperfusion; ukrain was intraperitoneally administered 1 h before the IR process). RESULTS: Serum total oxidant status (TOS) and total antioxidant status (TAS) levels were measured. The oxidative stress index was determined by calculating the TOS/TAS ratio. TAS serum levels significantly increased, and TOS serum levels also prominently decreased in U + IR group, when compared with the IR group (P < 0.001). Mean NGAL level was remarkably higher in IR group, when compared with the U + IR group (P < 0.001). Caspase-3 messenger RNA (mRNA) expression level increased in IR and decreased in U + IR group (P < 0.001). Bcl-xL serum and mRNA expression levels increased in the U + IR group (P < 0.001). In addition, serum iNOS and mRNA expression levels increased in IR group and decreased in U + IR group (P < 0.001). CONCLUSIONS: Data established from the present study suggest that ukrain may exhibit protective effect against IR-induced kidney injury and that antioxidant activity primarily modulates this effect.

The effect of adropin on lipid and glucose metabolism in rats with hyperlipidemia.

OBJECTIVES: The aim of this study was to evaluate, for the first time, whether the effects of low-dose adropin administration is effective in rats with hyperlipidemia. MATERIALS AND METHODS: Twenty one Wistar albino female rats were randomly divided into 3 groups and fed with high-fat diet for 4 weeks to establish the hyperlipidemia model. Meanwhile, adropin was administrated intraperitonealy (2.1 µg/kg/day), once a day for continuous 10 days. Then, body weights and serum biochemical parameters, adropin, insulin and blood glucose levels were determined. Additionally, in liver tissue, inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) mRNA gene expressions were evaluated by RT-PCR. RESULTS: The results showed that intraperitoneal administration of adropin to hyperlipidemic rats for 10 days were extremely effective in decreasing the levels of serum triglycerides (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and gamma glutamil transferase (GGT) and increasing the levels of high density lipoprotein cholesterol (HDL-C). It could decrease mRNA expressions of pro-inflammatory cytokines TNF-α and IL-6 via regulating the expressions of iNOS. In addition, treatment with adropin showed a significant reduction in blood glucose, serum insulin levels, HbA1c (%), and HOMA-IR, and increase in serum adropin levels. CONCLUSION: Adropin may ameliorate lipid metabolism, reduce insulin resistance, and inhibit hepatocytes inflammation. Thus, adropin had significant therapeutic benefits and could be suggested as a potential candidate agent against hyperlipidemia.

Antiadhesive and anti-inflammatory effects of pirfenidone in postoperative intra-abdominal adhesion in an experimental rat model.

BACKGROUND: Pirfenidone (PF) is a potent antifibrotic and anti-inflammatory agent. We investigated the protective effect of PF against postoperative intra-abdominal adhesions. MATERIAL AND METHODS: Thirty male Sprague-Dawley rats were divided into three groups (n = 10 in each group). In group 1 (control), adhesion induction was performed by cecal abrasion, and no treatment was administered. In group 2 (vehicle), for 2 wk after adhesion induction, 0.4%-carboxymethylcellulose was administered by gavage. In group 3 (PF treatment), for 2 wk after adhesion induction, 500-mg/kg/d PF was administered by gavage. On the 15th postoperative day, the animals were killed, and cecal and peritoneal tissues were excised. The adhesions were graded macroscopically. The protein concentrations and mRNA expression levels of the following genes were measured in the tissues: matrix metallopeptidase-9 (MMP-9); tissue inhibitor of metalloproteinase-1 (TIMP-1); tumor necrosis factor-alpha (TNF-α); and transforming growth factor-beta 1 (TGF-ß1). The tissue samples were also evaluated histopathologically. RESULTS: Macroscopic and histopathologic evaluation showed that PF-reduced adhesion and inflammation (P < 0.001, P = 0.004, respectively). Pretreatment with PF-reduced TIMP-1, TNF-α, and TGF-ß1 protein concentrations (P < 0.001, P < 0.001, and P < 0.001, respectively) and mRNA expression levels (P = 0.030, P = 0.005, and P = 0.016, respectively) and increased MMP-9 protein concentrations (P < 0.001) and mRNA expression (P = 0.021). CONCLUSIONS: The findings of this study suggest that PF can be used as a protective agent to prevent the development of peritoneal adhesions and inflammation during the postoperative period.

Ukrain (NSC 631570) ameliorates intestinal ischemia-reperfusion-induced acute lung injury by reducing oxidative stress.

Intestinal ischemia-reperfusion (I/R) causes severe destruction in remote organs. Lung damage is a frequently seen complication after intestinal I/R. Ukrain (NSC 631570) is a synthetic thiophosphate derivative of alkaloids from the extract of the celandine (Chelidonium majus L.) plant. We investigated the effect of Ukrain in animals with lung injury induced by intestinal I/R. Adult male Spraque-Dawley rats were randomly divided into four groups: control, Ukrain, I/R, I/R with Ukrain. Before intestinal I/R was induced, Ukrain was administered intraperitoneally at a dose of 7.0 mg/body weight. After 1 h ischemia and 2 h reperfusion period, lung tissues were excised. Tissue levels of total oxidative status (TOS), total antioxidant status (TAS) were measured and oxidative stress indices (OSI) were calculated. Lung tissues were also examined histopathologically. TOS and OSI levels markedly increased and TAS levels decreased in the I/R group compared to the control group (P < 0.05). TOS and OSI levels markedly decreased and TAS levels increased in the I/R with Ukrain group compared with the group subjected to IR only (P < 0.05). Severe hemorrhage, alveolar septal thickening, and leukocyte infiltration were observed  in the I/R group. In the I/R with Ukrain group, morphologic changes occurring as a result of lung damage attenuated and histopathological scores reduced compared to the I/R group (P < 0.05). Our results suggest that Ukrain pretreatment could reduce lung injury induced by intestinal I/R induced via anti-inflammatory and antioxidant effects.

Molecular and biochemical evidence on the protective effects of embelin and carnosic acid in isoproterenol-induced acute myocardial injury in rats.

AIMS: Acute myocardial infarction is a serious acute cardiac disorder and heart disease is still a major public health problem in adults. We investigated the effects of embelin (EMB) and carnosic acid (CA) in animals with isoproterenol (ISO)-induced myocardial injury. MAIN METHODS: Adult male Wistar-Albino rats were divided into four groups: control, ISO, ISO with EMB, and ISO with CA. Before myocardial injury was induced, drugs were administered by oral gavage. Myocardial injury was induced by subcutaneous injection of ISO hydrochloride for 2 consecutive days. Serum cardiac troponin I (cTnI), ischemia modified albumin (IMA), heart fatty acid binding protein (HFABP) levels and paraoxonase-1 (PON-1) activity, tissue total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), tumor necrosis factor-α (TNF-α) levels, superoxide dismutase (SOD) activity, and glutathione peroxidase (GSH-Px) activity were measured. Tissue mRNA expression levels of nuclear factor-kappa B (NF-κB), P38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor erythroid 2-related factor 2 (Nrf2) were analyzed. In addition, cardiac tissues were evaluated histopathologically and immunohistochemically. KEY FINDINGS: All tested compounds reduced myocardial damage, apoptosis, cTnI, IMA, HFABP, TOS, and TNF-α levels, NF-κB, p38 MAPK, and phosphorylated c-Jun N-terminal protein kinase (pJNK 1/2) expressions. All tested compounds increased SOD activity, GSH-Px activity, TAS levels, TT levels, phosphorylated extracellular signal-regulated kinase (pERK 1/2), and Nrf2 expressions. SIGNIFICANCE: Our results suggest that EMB and CA pretreatment could reduce myocardial injury via antiinflammatory, antioxidant, and antiapoptotic effects.

Effects of captopril, telmisartan and bardoxolone methyl (CDDO-Me) in ischemia-reperfusion-induced acute kidney injury in rats: an experimental comparative study.

Renal ischemia-reperfusion (IR) injury is one of the most common causes of acute kidney injury. This study investigated the effects of captopril (CAP), telmisartan (TEL) and bardoxolone methyl (BM) in animals with renal IR injury. Adult male Wistar-Albino rats were divided into six groups: control, vehicle, IR, IR with CAP, IR with TEL and IR with BM. Before IR was induced, drugs were administered by oral gavage. After a 60-min ischemia and a 120-min reperfusion period, bilateral nephrectomies were performed. Serum urea, creatinine, neutrophil gelatinase-associated lipocalin (NGAL) levels, tissue total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), asymmetric dimethylarginine (ADMA) levels, superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-Px) activity were measured. Tissue mRNA expression levels of peroxisome proliferator-activated receptor-É£ (PPAR-É£), nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were analyzed. In addition, renal tissues were evaluated histopathologically and immunohistochemically. All tested drugs reduced renal damage, apoptosis, urea, creatinine, NGAL, TOS, nitric oxide (NO) and ADMA levels, NF-κB, inducible nitric oxide synthase (iNOS) and endothelin-1 (ET-1) expressions (P < 0.001). All tested drugs increased SOD activity, GSH-Px activity, TAS levels, TT levels, endothelial nitric oxide synthase (eNOS) expression, dimethylarginine dimethylaminohydrolases (DDAHs) expression, Nrf2 expression and PPAR-É£ expression (P < 0.001, P < 0.003). These results suggest that CAP, TEL and BM pretreatment could reduce renal IR injury via anti-inflammatory, antioxidant and anti-apoptotic effects.

The effect of ozone on blood pressure in DOCA-salt-induced hypertensive rats.

BACKGROUND: Hypertension is a risk factor for the cardiovascular diseases. Ozone as a therapeutic agent for the treatment of several disorders. We aimed to observe the effects of ozone on the blood pressure in DOCA-salt hypertensive rats. METHODS: Twenty three young Sprague Dawley male rats were divided into three groups; Control (C), Hypertension (H) and Hypertension + Ozone (HO). Hypertension was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly, 4 weeks, whereas intraperitoneal ozone was administered (1.1 mg/kg) for 10 days. Serum endothelin-1, nitric oxide and renin levels were measured with ELISA. Blood pressures were monitored using a tail cuff system. Endothelin-1, ET receptor A and ET receptor B mRNA expression in heart and vascular tissue were assessed by quantitative reverse transcription polymerase chain reaction. RESULTS: Blood pressure, serum endothelin-1 and ET receptor A mRNA expression levels were increased in H group, whereas serum renin, nitric oxide and ET receptor B mRNA expression levels in the heart and vascular tissue decreased compared with C and HO groups, which were counteracted by ozone treatment. CONCLUSION: Ozone treatment decreases blood pressure and is effective in preventing the progression of hypertensive disease, the mechanisms of which are associated with anti-vasoconstrictor effects through reducing the levels of serum endothelin-1 and ET receptor A mRNA expression in the heart and vascular tissue.