Dose Of Olive Oil Research Articles

Study on mechanism of salidroside against liver fibrosis by regulating CXCL16

In order to investigate the effect of salidroside on inhibiting liver fibrosis and its relationship with CXC chemokine ligand 16(CXCL16) in vivo and in vitro, totally 45 C57 BL/6 J male mice were randomly divided into normal group, model group and salidroside group, with 15 mice in each group. The mice in model group and salidroside group were injected intraperitoneally with 15% carbontetrachloride(CCl_4) olive oil solution to establish liver fibrosis model, and the mice in normal group were injected intraperitoneally with the same dose of olive oil. Salidroside group was given with 100 mg·kg~(-1 )salidroside by gavage, while the normal group and model group received the same amount of double distilled water by gavage. All mice were sacrificed after 5 weeks of intragastric administration. The pathological changes of mouse liver were observed by hematoxylin-eosin(HE) staining, and the degree of liver fibrosis was observed by sirius red staining. The protein expressions of collagen Ⅰ(ColⅠ), α-smooth muscle actin(α-SMA), fibronectin(FN), CXCL16, phosphorylated Akt(p-Akt), Akt in liver tissues were detected by Western blot. Hepatic stellate cell line JS 1 was cultured in vitro and divided into control group, model group(100 μg·L~(-1) CXCL16) and salidroside group(100 μg·L~(-1) CXCL16+1×10~(-5) mol·L~(-1) salidroside). Cell migration was detected by cell scratch, the mRNA expressions of ColⅠ and α-SMA were detected by RT-PCR, and the protein expressions of p-Akt and Akt were detected by Western blot. As compared with the normal group, the protein expressions of ColⅠ, α-SMA, FN, CXCL16, and p-Akt in the model group were significantly increased, and salidroside could reduce the expression of these indicators(P<0.05 or P<0.01). In vitro, CXCL16 could promote the migration of JS 1, increase the mRNA expressions of ColⅠ and α-SMA in JS 1, and enhance Akt phosphorylation in JS 1(P<0.05 or P<0.01). As compared with the model group, salidroside could inhibit the migration of JS 1 induced by CXCL16(P<0.05), and reduce the high expression of ColⅠ and α-SMA mRNA and the phosphorylation of Akt in JS 1 induced by CXCL16(P<0.05). In conclusion, salidroside might attenuate CCl_4-induced liver fibrosis in mice by inhibiting the migration, activation and Akt phosphorylation of hepatic stellate cells induced by CXCL16.

Protective Effect of Organic Selenium on Oxidative Damage and Inflammatory Reaction of Rabbit Kidney Induced by T-2 Toxin.

T-2 toxin is a member of a class of mycotoxins produced by a variety of Fusarium species under appropriate temperature and humidity conditions and is a common contaminant in food and feedstuffs of cereal origin. Selenium is an indispensable element in animals, regulates a variety of biological functions of the body, and can antagonize metal and mycotoxin poisoning to a certain extent. However, the effect of selenium on kidney injury induced by T-2 toxin has not been reported. In this study, 50 New Zealand rabbits were divided into 5 groups (the control group, T-2 toxin group, low-dose Se + T-2 toxin group, medium-dose Se + T-2 toxin group, and high-dose Se + T-2 toxin group). Rabbits were examined after oral administration of different doses of selenomethionine (SeMet) for 21days and after perfusion with 0.4mg/kg T-2 toxin (or the same dose of olive oil in the control group) for 5days. We found that T-2 toxin induced kidney function damage and increased the levels of ROS and the contents of inflammatory factors. Renal structure was pathologically damaged. However, we found that after pretreatment with 0.2mg/kg SeMet, oxidative stress, the inflammatory response, and pathological damage induced by T-2 toxin were attenuated. The results indicate that a low dose (0.2mg/kg) of SeMet effectively reversed T-2 toxin-induced kidney injury in rabbits.

Diagnostic value of diffusion kurtosis imaging in assessing liver fibrosis

Objective To investigate the diagnostic value of diffusion kurtosis imaging(DKI)in the classification of hepatic fibrosis. Methods Thirty-five male SD rats were randomly divided into two groups: the hepatic fibrosis group(n=28)and the control group(n=7). The rats in hepatic fibrosis group were randomly divided into 4 subgroups and seven rats per group, the rats were administrated 50% CCl4 intraperitoneally twice a week to establish hepatic fibrosis, and the four subgroups were injected 2, 4, 6, and 8 weeks, respectively. The rats in the control group were administrated same dose of olive oil for 8 weeks. One rat in hepatic fibrosis group was died of liver failure in the 7th week, and a total of 27 fibrosis experimental rats and 7 control rats were finally included in this study. DKI was performed at the end of the injection period for all rats, the apparent diffusion(D)and kurtosis(K)values were evaluated. Rats were sacrificed immediately after MRI scan and liver specimens were collected. The liver tissues were examined by pathology, liver fibrosis degree, which was graded from S0 to S4, and inflammatory activity, which was graded from G0 to G3 were graded. The difference of D value and K value between different liver fibrosis and inflammatory activity scores was compared by one-way ANOVA(normal distribution)or Kruskal-Wallis test(skewed distribution). Spearman correlation analysis and multiple regression analysis were used to reveal the correlation between DKI parameters and fibrosis staging/necroinflammatory activity grade. To confirm the efficiency of using the ROC curve of DKI parameters to qualify the liver fibrosis grade, which grade was≥ 3. Results Seven, 6, 6, 7, 8 rats were diagnosed as S0 to S4, respectively. The difference of D value and K value among different fibrosis grades was statistically significant(P<0.05). D value and the degree of fibrosis was negatively correlated(r=-0.650, P<0.01);K value and liver fibrosis grade no correlation(r=0.336, P=0.080). Thirteen, 6, 8, 7 rats were diagnosed as G0 to G3, respectively. D value was negatively correlated with inflammatory activity(r=-0.590, P=0.001);K value was no correlation with inflammatory activity(r=0.169, P=0.389). Compared with inflammatory activity, fibrosis classification was an independent factor in determining D values(P=0.001). ROC analyses demonstrated an area under the curve(AUC)of D value, K value, D value combined with K value in the diagnosis of liver fibrosis grading ≥ 3 level were 0.781, 0.672 and 0.833, respectlively. The sensitivity and specificity of D value combined with K value were 83.3% and 75.0%, respectively. Conclusion DKI imaging is of great value in the classification of hepatic fibrosis and can be used as an effective method for the diagnosis of fibrosis. Key words: Liver cirrhosis; Magnetic resonance imaging; Comparative study

Up-regulation of components of the renin–angiotensin system in liver fibrosis in the rat induced by CCL4

The purpose of this study was to investigate the components of renin–angiotensin system (RAS), liver function and histology in liver fibrogenesis in the rats induced by low-dose chronic carbon tetrachloride (CCL4) administration and evaluate the relationship between biochemical variables and components of RAS. Male Sprague–Dawley (SD) rats were randomly divided into the CCL4 group which received intraperitoneal injection of 40% CCL4 dissolved in olive oil every three days for four consecutive weeks (Initial dose was 5mL/kg, other dose: 3mL/kg) and the control group which received the same dose of olive oil. The micro-structure of the liver was examined by H&E. Hepatic Ang II and Ang(1–7) was detected. Real-time PCR and Western-blot were performed to determine the gene and protein expression of the RAS. The components of RAS were all up-regulated in CCL4 group, and the increased extent of ACE-Ang II-AT1 axis was higher than the ACE2-Ang(1–7)-Mas axis. There was a significant correlation between ACE and ACE2 gene expression, AT1 and MAS gene expression, Ang II and Ang(1–7) in the liver of rats. ACE (or ACE2) gene expression strongly correlated with the index of liver injury significantly. These results suggest hepatic fibrogenesis induced by chronic CCL4 administration may be associated with the relationship of ACE-Ang II-AT1 axis and ACE2-Ang(1–7)-MAS axis.

Effect of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin suggests abnormal palate development after palatal fusion

Mouse embryos exposed to 2,3,7,8-tetrachloridedibenzo-p-dioxin (TCDD) develop cleft palates and hydronephrosis. Cleft palates occur after TCDD exposure due to contact and/or fusion failure. We investigated whether cleft palate can be induced by dissociation of the palatine process after fusion. Pregnant mice on gestational day (GD) 12 were randomly divided into two groups: one group was administered through gastric tubes one dose of olive oil (control group) and the other group was administered one dose of TCDD diluted with olive oil, both at a dose of 40 microg/kg body weight. Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 13-18) and the palatal form was observed using a stereoscopic microscope. In TCDD-exposed embryos, palatal fusion was observed on GD 14, 15 and 16 and the incidence of cleft palate was 100% on GD 18. Fusion rates were 17.5 +/- 15.2% and 12.4 +/- 11.8% on GD 15 and 16, respectively. Some palates from the TCDD-exposed mouse embryos showed clearly developed cleft palate after fusion of the lateral palatine processes during palatal formation. A mass of cells, which were chiefly epithelial in the fused palates was observed in the TCDD-exposed mouse embryos. A decrease in E-cadherin expression was observed in this mass of cells, indicating its involvement in the development of cleft palate.

The Antioxidant Effect of Rosa rugosa

We examined the effects of Rosa rugosa (Rosa rugosa Thunb) on lipid peroxidation, alanine transaminase (ALT), aspartate transaminase (AST), glutathione and protein oxidation levels in carbon tetrachloride (CCl4) treated male Wistar rats. Two control groups and one treatment group of rats were formed. The control groups were fed a standard diet, while the Rosa rugosa group was fed a standard diet enriched with 6% by weight dried Rosa rugosa fruit powder. After 3 months, a single dose of CCl4 was injected intraperitoneally in the Control II and Rosa rugosa groups (1 ml/kg, as 20% in olive oil) and a similar dose of olive oil was administered i.p. to rats in the Control I group. The rats were sacrificed 2 hours later. Lipid peroxide levels in liver, protein oxidation in liver, glutathione (GSH) levels in liver, and ALT and AST in plasma were measured. The rats in the Rosa rugosa group were found to have significantly lower liver peroxide, protein oxidation, glutathione levels and plasma ALT and AST activities compared with the rats in the CCl4 treated control group. These findings suggest that Rosa rugosa possesses antioxidant activity.

Expression of vasoactive mediators during mechanical ventilation in nitrofen-induced diaphragmatic hernia in rats

The high mortality in patients with congenital diaphragmatic hernia (CDH) has been attributed to pulmonary hypoplasia and persistent pulmonary hypertension (PPH). Endothelin-1 (ET-1), nitric oxide (NO), and calcitonin gene-related peptide (CGRP) have been reported to be important vasoactive mediators in the perinatal pulmonary circulation. The exact mechanism by which these vasoactive mediators interact to regulate the perinatal pulmonary vascular tone in CDH with PPH is not fully understood. We hypothesized that the altered pulmonary vascular reactivity in CDH is due to imbalance in vasoactive mediators. This study was designed to investigate mRNA expression of ET-1, eNOS, and CGRP in CDH lung in the perinatal period. A CDH model was induced in pregnant rats following administration of nitrofen. In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The newborn rats were intubated and ventilated, and ventilation was continued for 1-6 h. Left lungs were collected from both groups at 0, 1, and 6 h after ventilation (n=8 in each group). Reverse transcriptase-polymerase chain reaction on lung tissue was performed to evaluate the relative level of ET-1, eNOS, and CGRP mRNA expression. The results showed a significant increase in ET-1 mRNA in CDH lung at 1 and 6 h after ventilation compared with controls. In CDH lung, eNOS mRNA and CGRP mRNA levels were significantly increased at 1 h but were similar to control values at 6 h after ventilation. The increased expression of vasoconstrictor ET-1 mRNA and vasodilators eNOS mRNA and CGRP mRNA in the CDH lung at 1 h after ventilation suggests that pulmonary vascular tone is rapidly changing after birth. An imbalance in the production of vasoconstrictors and vasodilators by the CDH lung may contribute to high pulmonary vascular resistance.

Photodegradation of polychlorinated dibenzo-p-dioxins and dibenzofurans in soil with vegetable oil.

This study was carried out to investigate the effect of olive oil on the photodegradation of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in contaminated sawmill soil. Previous studies had shown that the solubility of PCDD/Fs in olive oil is high and a rapid photodegradation of PCDD/Fs takes place in olive oil when irradiated with ultraviolet (blacklight) lamps. The efficiency of this treatment method was evaluated under more practical conditions. These included the use of sunlight irradiation and a lower-grade olive oil, without a preliminary extraction of soil with olive oil. A 1-cm layer of contaminated sawmill soil was blended with 20 weight-% of olive oil and exposed to sunlight for four weeks. In another experiment, a new dose of olive oil was added at the middle of the exposure period. The PCDD/F concentrations of the soils were monitored periodically. A reduction in the concentration of 2,3,7,8-chlorinated PCDD/Fs by 59% and in WHO-TEQ in contaminated sawmill soil by 48% was attained after blending the soil with two doses (20 + 20%) of olive oil and exposing the mixture to sunlight for four weeks. Photodegradation with only one dose of olive oil was less efficient. This suggests that periodical additions of olive oil would be needed to maintain a proper degradation rate. After the oil additions, the WHO-TEQ content of the soil declined with first order reaction half-lives of 19.2 to 19.7 d. The overall half-life during the four-week treatment, however, was 30 d. A significant reduction in the PCDD/F concentration of aged sawmill soil can be achieved with a relatively simple olive oil-sunlight treatment. Some theoretical and technological questions need to be solved before using the investigated soil decontamination method in larger-scale applications. The functions of vegetable oils in photodegradation processes should be studied in more detail. The amount of oil that is needed for a proper solubilisation and photodegradation of PCDD/Fs should be minimised. Moreover, special care should be taken to prevent mobilisation of PCDD/Fs to the surrounding environment and to avoid leaving bioavailable residuals of PCDD/Fs in soil.

Gene expression of fibroblast growth factors 10 and 7 is downregulated in the lung of nitrofen-induced diaphragmatic hernia in rats

Background/purpose Newborns with congenital diaphragmatic hernia (CDH) still have a high mortality rate, which has been attributed to pulmonary hypoplasia and pulmonary hypertension. Fibroblast growth factors (FGFs) are essential components of the gene network that regulates lung development. Recent studies suggest that the new member of FGF family, FGF-10, plays a fundamental role in branching morphogenesis and is essential for lung formation. FGF-10-deficient mice exhibit complete absence of lungs. FGF-7 promotes epithelial proliferation and expansion leading to the formation of cystlike structures. The aim of this study was to determine the gene level expression of FGF-10 and FGF-7 in the lung of nitrofen-induced CDH. Methods Congenital diaphragmatic hernia (CDH) was induced in pregnant rats after administration of 100 mg of nitrofen on day 9.5 of gestation (term, 22 days). In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into 3 groups: normal controls (n = 16), nitrofen induced without CDH (n = 16), and nitrofen-induced CDH (n = 16). Total RNA and DNA were extracted from the lung in each group and measured. mRNA was extracted from total RNA. Reverse transcription polymerase chain reaction (RT-PCR) was performed to evaluate mRNA expressions of FGF-10 and FGF-7. Levels of mRNA were expressed as a ratio of the band density divided by that of β-actin, a house-keeping gene. Results FGF-10 mRNA expression was decreased significantly in CDH lung (2.914 ± 0.320) compared with controls (4.062 ± 0.307; P < .05) and nitrofen induced without CDH lung (3.923 ± 0.250; P < .01). FGF-7 mRNA expression was decreased significantly in CDH lung (0.777 ± 0.097) compared with controls (1.028 ± 0.093; P < .01). Conclusions Decreased gene expression of FGF-10 and FGF-7 in the hypoplastic lung suggests that pulmonary hypoplasia in nitrofen-induced CDH rat may be caused by reduced synthesis of FGF-10 and FGF-7 during lung morphogenesis.

Increased expression of ICAM-1 and VCAM-1 in the lung of nitrofen-induced congenital diaphragmatic hernia in rats.

Recently, increased expression of inflammatory cytokine, tumor necrosis factor (TNF)-alpha, has been reported in both humans and animal models with CDH and the decreased TNF-alpha expression in CDH lung after antenatal dexamethasone (Dex) treatment. Intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 are induced by several inflammatory cytokines such as TNF-alpha. The aim of this study was to investigate pulmonary ICAM-1 and VCAM-1 expression in CDH lung in rats and to determine the effect of antenatal glucocorticoid. CDH model was induced in pregnant rats following administration of nitrofen on day 9.5 of gestation. In control animals, the same dose of olive oil was given without nitrofen. Dex (0.25 mg/kg) was given on day 18.5 and 19.5 of gestation. RT-PCR was performed to evaluate the relative amount of ICAM-1 and VCAM-1 mRNA expression. Fluorescein immunohistochemistry using anti-ICAM-1 and anti-VCAM-1 antibody was performed using light and confocal microscopy. ICAM-1 and VCAM-1 mRNA expression and ICAM-1 and VCAM-1 immunoreactivity were markedly increased in CDH lung compared to controls. Dex downregulated the expression of both adhesion molecules in the hypoplastic lung. Increased ICAM-1 and VCAM-1 mRNA expression in hypoplastic lungs would suggest that the increased local synthesis of pulmonary adhesion molecules may induce respiratory distress in CDH. Decreased expression of adhesion molecules in CDH lungs after Dex treatment suggests that antenatal glucocorticoids therapy may improve pulmonary immaturity and associated respiratory distress in nitrofen-induced CDH lung.

Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1: expression in the lung of fetal rats with nitrofen-induced diaphragmatic hernia.

The surrounding extracellular matrix of airway wall tissues changes in response to mechanical stresses and hypoxia. The presence of matrix metalloproteinase-9 (MMP-9) and its inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1), is correlated with collagen degradation and tissue repair in lung disorders. The aim of this study was to evaluate the expression of MMP-9 and TIMP-1 in the lung of fetal rats with nitrofen-induced congenital diaphragmatic hernia (CDH). Administering 100 mg of nitrofen dissolved in 1 ml olive oil to pregnant Wistar rats on day 9 of gestation induced left-sided CDH in fetal rats. In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into two groups: normal controls (n = 10) and nitrofen-induced left-sided CDH (n = 10). Immunoreactivity of the staining for MMP-9 and TIMP-1 in the lung tissues was semiquantitatively analyzed using the staining scores. The relative amount of MMP-9 or TIMP-1 divided by the amount of beta-actin for each lung sample was measured by using the real-time reverse-transcriptase polymerase chain reaction. The immunoreactivity of MMP-9 was significantly increased in the CDH group (n = 5) compared with the control group (n = 5) (p = 0.031). On the other hand, the immunoreactivity of TIMP-1 in the two groups was not significantly different (n = 0.134). The relative amount of MMP-9 (or TIMP-1) in the CDH group (n = 5) does not differ significantly from that in the control group (n = 5) (p = 0.059, 0.596, respectively), but the relative amount of MMP-9 is higher in the CDH group, although it is not significantly higher. On the other hand, the ratios of MMP-9 to TIMP-1 were significantly higher in the CDH group (p = 0.028). In conclusion, fetal rats with nitrofen-induced CDH, a model of respiratory disorders, manifested the excess of MMP-9 activity due to the absence of TIMP-1 that would suggest a trend toward disruption of the extracellular matrix in the CDH lung tissues.

Gene expression of insulin-like growth factor-1 and epidermal growth factor is downregulated in the heart of rats with nitrofen-induced diaphragmatic hernia.

Newborns with congenital diaphragmatic hernia (CDH) still have high mortality. Recently, a possible role of cardiac maldevelopment has been suggested. Human and experimental studies have demonstrated that heart weight is significantly reduced in the presence of CDH. Recent studies have suggested an important role for insulin-like growth factor-I (IGF-I) in the regulation of cardiac growth, structure, and function. Administration of IGF-I to normal rats has been shown to cause cardiac hypertrophy. Epidermal growth factor (EGF) plays an important role in cardiac differentiation and development. The aim of this study was to determine the gene-level expression of IGF-I and EGF in the hearts of rats with nitrofen-induced CDH using the reverse-transcription polymerase chain reaction technique (RT-PCR). CDH was induced in pregnant rats following administration of 100 mg nitrofen on day 9.5 of gestation (term 22 days). In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into three groups: normal controls (n = 8), nitrofen without CDH (n = 8), and nitrofen-induced CDH (n = 8). Total RNA was extracted from the hearts in each group and measured. mRNA was extracted from total RNA. RT-PCR was performed to evaluate mRNA expressions of IGF-I and EGF. Levels of mRNA were expressed as a ratio of band density divided by that of beta-actin, a housekeeping gene known to be expressed at a constant level. IGF-I mRNA expression was significantly decreased in CDH hearts (0.177 +/- 0.109) compared to controls (0.393 +/- 0.138) (P < 0.01) and nitrofen hearts without CDH (0.321 +/- 0.088) (P < 0.05). EGF mRNA expression was significantly decreased in CDH hearts (0.218 +/- 0.118) compared to controls (0.534 +/- 0.196) (P < 0.01) and nitrofen hearts without CDH (0.383 +/- 0.136) (P < 0.05). Decreased cardiac gene expression of IGF-I and EGF in the hypoplastic heart suggests that cardiac hypoplasia in nitrofen-induced rat CDH may be due to reduced synthesis of IGF-I and EGF by myocytes in the developing heart.

Structural immaturity of the heart in congenital diaphragmatic hernia in rats

Purpose: The form and function of the heart are the final result of an integration of cells, tissues, and extracellular material. The extracellular matrix (ECM) is a complex array of different molecular components, and it plays an important role for the transfer of mechanical force in both contraction and relaxation phases in the cardiac cycle. ECM plays also a significant role in the development of the heart. The aim of this study was to evaluate the expression of important ECM components in the heart of rats with induced CDH to test the hypothesis that an alteration of ECM may contribute to the cardiac maldevelopment, which recently has been identified as a contributive factor for the high mortality rate in babies with congenital diaphragmatic hernia (CDH). Methods: CDH model was induced in pregnant rats after administration of 100 mg of nitrofen on day 9.5 of gestation (term, 22 days). In control animals the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into 2 groups: normal control (n = 10) and nitrofen-induced CDH (n = 10). Reverse transcription polymerase chain reaction (RT-PCR) was performed to evaluate the relative amount of tropoelastin and α1 (I) procollagen mRNA expression. Elastin protein content was measured using enzyme-linked immunosorbent assay (ELISA). Results: There was a reduction in tropoelastin mRNA (P <.05) and procollagen mRNA (P <.05) in CDH compared with controls. The cardiac α-elastin content also was reduced in CDH (P <.01). Conclusions: The reduced cardiac tropoelastin and procollagen gene expression and the reduced α-elastin content indicate that the heart in CDH structurally is immature. The reduced production of cardiac ECM may contribute to a contractile dysfunction, which makes the heart unable to respond to the hemodynamic load accompanying persistent pulmonary hypertension (PPH). J Pediatr Surg 36:770-773. Copyright © 2001 by W.B. Saunders Company.

The hypoplastic heart in congenital diaphragmatic hernia: reduced expression of basic fibroblast growth factor and platelet-derived growth factor.

Newborn infants with congenital diaphragmatic hernia (CDH) still have high mortality. Recently, the possible role of a cardiac maldevelopment in the high mortality has been suggested. Human and animal studies have demonstrated that heart weight is significantly reduced in the presence of CDH. Basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) are pleiotropic regulatory peptides that are expressed in myocardium in precise developmental and spatial programs. PDGF and bFGF both stimulate cardiac growth by inducing cell proliferation and stimulating the synthesis of extracellular matrix. The aim of this study was to investigate the presence of heart hypoplasia in nitrofen-induced CDH in rats and the role of specific tissue growth factors (bFGF and PDGF) in its genesis. CDH was induced in pregnant rats following administration of 100 mg nitrofen on day 9.5 of gestation (term 22 days). In control animals the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided in two groups: normal controls (n = 8) and nitrofen-induced CDH (n = 8). Total RNA, DNA, and soluble proteins were extracted from the heart in each group and measured. mRNA was extracted from total RNA and a reverse transcription-polymerase chain reaction (RT-PCR) was performed to evaluate mRNA expression of bFGF and PDGF. The heart/body weight ratio (HBWR) and DNA content were significantly decreased (P < 0.01) in CDH animals compared to controls. RNA and protein content were also reduced in CDH. The expression of bFGF and PDGF mRNA was significantly reduced in the CDH group compared to controls (P < 0.01). The decreased HBWR, DNA, RNA, and protein content in the CDH heart indicates that the heart is hypoplastic in nitrofen-induced left CDH. The downregulation of bFGF and PDGF gene expression in the CDH heart suggests that these regulating peptides may play an important role in the genesis of cardiac hypoplasia in CDH.