Reduction of oxidative stress and apoptosis in hyperlipidemic rats by composite oil (CO) of Sesamum indicum L. and Vicia faba L.

2021 ◽  
pp. 1-11
Author(s):  
Holima Khatun ◽  
Mousumi Mitra ◽  
Koushik Das ◽  
Atiskumar Chattopadhyay ◽  
Dilip Kumar Nandi
Keyword(s):  
Oxidative Stress ◽  
Vicia Faba ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Seed Oil ◽  
Treated Group ◽  
Ros Generation ◽  
Group Iii ◽  
Tnf Α ◽  
Group Ii

BACKGROUND: Hyperlipidemia associated with cardiovascular diseases (CVDs) is a global health issue that can be alleviated by functional foods. OBJECTIVES: The present study aimed to investigate the effect of composite oil (CO) of sesame seed oil (SSiO) and Vicia faba seed oil (SVfO) on inflammatory factors, ROS generation level, and cell apoptosis level on high lipid diet (HLD) induced hyperlipidemic rat model. METHODS: Hyperlipidemic rat model was developed by feeding HLD to the experimental rats for eight weeks. Male albino rats weighing around 200–210 g were randomly divided into three equal groups: group I: control, received a normal diet; group II: received HLD for eight weeks, group III: received the HLD with CO orally. After 60 days of treatment, the levels of C-reactive protein (CRP), interleukin (IL)-10; tumor necrosis factor (TNF)-α, IL-18, reactive oxygen species (ROS), and cell apoptosis were serially assessed. RESULTS: After eight weeks of CO treatment, TNF- α, IL-18, CRP, and oxidative ROS generation significantly decreased in CO treated group (group III) compared to group II. On the other hand, IL-10 levels significantly increased in CO treated group compared to group II animals. It was also observed that the percentage of the late apoptotic cell reduced considerably in the CO treated group (group III) compared to HLD-fed animals (group II). CONCLUSION: The results indicate that the CO could prevent CVDs via suppressing oxidative stress, ameliorating inflammation and apoptosis in hyperlipidemic rats.

scholarly journals Effect of caraway on gentamicin-induced oxidative stress, inflammation and nephrotoxicity in rats

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Hoda Erjaee ◽  
Fatemeh Azma ◽  
Saeed Nazifi
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Group Treatment ◽  
Structural Damage ◽  
Seed Oil ◽  
Treated Group ◽  
Control Group ◽  
Protective Effects ◽  
Simultaneous Treatment ◽  
Tnf Α

Different potentially therapeutic approaches to prevent or attenuate gentamicin (GEM) induced nephrotoxicity have been proposed. The aim of the present study was to investigate the possible protective effects of caraway seed oil against GEM-induced nephrotoxicity in rats. Rats (24) were randomly assigned into four equal groups: i) normal control group, ii) treated with GEM, iii) pretreated with orally caraway seed oil 10 (mg kg−1) plus GEM and iv) treated with GEM and caraway seed oil 10 mg kg−1. Biochemical examinations were utilized for evaluation of the oxidative stress and renal nephrotoxicity. Creatinine, blood urea nitrogen (BUN), plasma malondialdehyde (MDA) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined. Administration of gentamicin to rats induced a marked renal failure, characterized by a significant increase in plasma creatinine and BUN concentrations. The animals treated with gentamicin alone showed a significantly higher plasma MDA level andlower SOD, GSH-Px and CAT activities when compared with the control group. Treatment and simultaneous treatment with caraway seed oil produced amelioration in MDA and increased the activity of antioxidant enzymes SOD, GSH-Px and CAT when compared with the gentamicin treated group. In addition, GEM nephrotoxicity increased renal inflammatory cytokines (TNF-α, IL-6 and IFN-γ). Pro-inflammatory cytokines were significantly decreased (P<0.05) in the test groups administered caraway seed oil. These findings suggest that caraway seed oil treatment attenuates renal dysfunction and structural damage through the reduction of oxidative stress and inflammation in rats.

scholarly journals The Effects of Asthma on the Stress Oxidative, Inflammation, and Endothelial Dysfunction Characteristics in Children with Severe Community-Acquired Pneumonia

2021 ◽  
Author(s):  
Ali Arjmand Shabestari ◽  
Pegah Mohaghegh ◽  
Habibeh kiyanrad ◽  
fatemeh imanparast
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Community Acquired Pneumonia ◽  
Healthy Children ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii ◽  
Stress Oxidative ◽  
Pai 1

Abstract Background: Pulmonary vascular endothelial activation, inflammation, and stress oxidative have been implicated in adverse clinical outcomes of community-acquired pneumonia (CAP). Although chronic lung problems such as asthma may affect the consequences of pneumonia, the exact mechanism of this effect remains unclear. The present study aimed to assess the effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction biomarkers in children pneumonia.Methods: This cross-sectional study was performed at Amir Kabir Hospital affiliated to Arak University of Medical Sciences, Arak, Iran. Participants were 25 children with severe CAP and asthma (group I), 25 children with severe CAP (group II), and 25 healthy children (group III) with 2 to 6 years of age. Fasting blood samples were taken to the assay of serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and Plasminogen activator inhibitor-1 (PAI-1).Results: We observed a significant reduction in TAC in groups I and II (0.997±0.22 and 1.23±0.21 mmol/l, respectively) compared with group III (1.46±0.19 mmol/l). This reduction was significantly higher in group I than in group II. Also, we observed a significant increase in MDA and TNF-α in groups I (2.57±0.40 µmol/l, 6.94±1.61 pg/ml, respectively) and II (6.94±1.61µmol/l, 5.54±1.84 pg/ml, respectively) compared with group III (1.89 ±0.27µmol/l, 3.42±1.32 pg/ml, respectively). The increase in MDA was significantly higher in group I than in group II. VCAM-1 and PAI-1 as endothelial dysfunction biomarkers increased significantly in group I (1.5 ±0.62 mmol/l and 10.52±3.2 AU/ml, respectively) compared with groups II (1.06±0.53 mmol/l and 8.23±3.4 AU/ml, respectively) and III (0.6± 0.35 mmol/l and 2.39 ± 0.83 AU/ml, respectively). Also, VCAM-1 and PAI-1 increased significantly in group II compared with groups III.Conclusions: Asthma can exacerbate the consequences of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction.

scholarly journals The Effects of Asthma on the Stress Oxidative, Inflammation, and Endothelial Dysfunction Characteristics in Children with Severe Community-Acquired Pneumonia

2021 ◽  
Author(s):  
ali Arjmand Shabestari ◽  
fatemeh imanparast ◽  
pegah mohaghegh ◽  
habibeh kiyanrad
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Community Acquired Pneumonia ◽  
Healthy Children ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii ◽  
Stress Oxidative ◽  
Pai 1

Background: Pulmonary vascular endothelial activation, inflammation, and stress oxidative have been implicated in adverse clinical outcomes of community-acquired pneumonia (CAP). Chronic lung problems such as asthma may affect the consequences of pneumonia.The present study aimed to assess the effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction biomarkers in children pneumonia. Methods: This cross-sectional study was performed at Amir Kabir Hospital affiliated to Arak University of Medical Sciences, Arak, Iran. Participants were 25 children with severe CAP and asthma (group I), 25 children with severe CAP (group II), and 25 healthy children (group III) with 2 to 6 years of age. Fasting blood samples were taken to the assay of serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and Plasminogen activator inhibitor-1 (PAI-1). Results: We observed a significant reduction in TAC in groups I and II compared with group III. This reduction was significantly higher in group I than in group II. Also, we observed a significant increase in MDA and TNF-α in groups I and II compared with group III. The increase in MDA was significantly higher in group I than in group II. VCAM-1 and PAI-1 as endothelial dysfunction biomarkers increased significantly in group I compared with groups II and III. Also, VCAM-1 and PAI-1 increased significantly in group II compared with groups III. Conclusions: Asthma can exacerbate the consequences of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction.

scholarly journals The Effects of Asthma on the Stress Oxidative, Inflammation, and Endothelial Dysfunction Characteristics in Children with Severe Community-Acquired Pneumonia

2020 ◽  
Author(s):  
Ali Arjmand Shabestari ◽  
Pegah Mohaghegh ◽  
Habibeh Kiyanrad ◽  
Fatemeh Imanparast
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Community Acquired Pneumonia ◽  
Healthy Children ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii ◽  
Stress Oxidative ◽  
Pai 1

Abstract Background: Pulmonary vascular endothelial activation, inflammation, and stress oxidative have been implicated in adverse clinical outcomes of community-acquired pneumonia (CAP). Although chronic lung problems such as asthma may affect the consequences of pneumonia, the exact mechanism of this effect remains unclear. The present study aimed to assess the effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction biomarkers in children pneumonia.Methods: This cross-sectional study was performed at Amir Kabir Hospital affiliated to Arak University of Medical Sciences, Arak, Iran. Participants were 25 children with severe CAP and asthma (group I), 25 children with severe CAP (group II), and 25 healthy children (group III) with 2 to 6 years of age. Fasting blood samples were taken to the assay of serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and Plasminogen activator inhibitor-1 (PAI-1).Results: We observed a significant reduction in TAC in groups I and II (0.997±0.22 and 1.23±0.21 mmol/l, respectively) compared with group III (1.46±0.19 mmol/l). This reduction was significantly higher in group I than in group II. Also, we observed a significant increase in MDA and TNF-α in groups I (2.57±0.40 µmol/l, 6.94±1.61 pg/ml, respectively) and II (6.94±1.61µmol/l, 5.54±1.84 pg/ml, respectively) compared with group III (1.89 ±0.27µmol/l, 3.42±1.32 pg/ml, respectively). The increase in MDA was significantly higher in group I than in group II. VCAM-1 and PAI-1 as endothelial dysfunction biomarkers increased significantly in group I (1.5 ±0.62 mmol/l and 10.52±3.2 AU/ml, respectively) compared with groups II (1.06±0.53 mmol/l and 8.23±3.4 AU/ml, respectively) and III (0.6± 0.35 mmol/l and 2.39 ± 0.83 AU/ml, respectively). Also, VCAM-1 and PAI-1 increased significantly in group II compared with groups III.Conclusions: Asthma can exacerbate the consequences of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction.

scholarly journals Ameliorating Effect of Combined Cinnamon and Ginger Oils against the Neurotoxicity of Nicotine Administration on the Prefrontal Cortex of Adult Albino Rats: Immunohistochemical and Ultrastructural Study

2021 ◽  
Vol 89 (3) ◽  
pp. 41
Author(s):  
Medhat Taha ◽  
Mohie Mahmoud Ibrahim ◽  
Mamdouh Eldesoqui ◽  
Mohamed A. M. Iesa ◽  
Tourki A. S. Baokbah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Group Iv ◽  
Tissue Homogenate ◽  
Control Group ◽  
Albino Rats ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii

Background: Nicotine is the active alkaloid in cigarettes. It was reported that tobacco smoking has many hazards; one of these hazards is the effect on the cognitive function of the prefrontal cortex. The aim of our study is to investigate the antioxidant effects of ginger, cinnamon oils, and their combination on morphological changes in the prefrontal cortex that were induced by nicotine. Materials and methods: Fifty adult male albino rats were divided into five groups: group I (control group), group II (nicotine), group III (nicotine + cinnamon), group IV (nicotine + ginger), and group V (nicotine + cinnamon + ginger). The coronal sections from the anterior part of the rat brain at the site of prefrontal cortex were examined by light microscope for (H&E and immunohistochemical staining with TNF-α and GFAP), while the ultrastructure morphology was examined by transmission electron microscopy. Levels of the oxidative stress markers (MDA, GSH) in the rats’ brain tissue homogenate were biochemically assessed. Results: Compared to the control group, the rats that were treated with nicotine (group II) showed a significant oxidative stress in the form of marked elevation of MDA and decrease in GSH, apoptotic changes especially in the pyramidal cells in the form of neuronal cell degeneration and pyknosis, and an elevation in the inflammatory marker TNF-α and GFAP expressions. These changes were observed to a lesser degree in rat group (III) and group (IV), while there was a marked improvement achieved by the combined usage of cinnamon and ginger oils, together compared to the nicotine group. Conclusions: Ginger and cinnamon are powerful antioxidants which ameliorate the degenerative and oxidative effects produced by nicotine on a rat’s prefrontal cortex.

scholarly journals Expression of miR-195 and its target gene Bcl-2 in human intervertebral disc degeneration and their effects on nucleus pulposus cell apoptosis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Xue-Lin Lin ◽  
Zhao-Yun Zheng ◽  
Qing-Shan Zhang ◽  
Zhen Zhang ◽  
You-Zhi An
Keyword(s):  
Cell Proliferation ◽  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Intervertebral Disc Degeneration ◽  
Target Gene ◽  
Blank Group ◽  
Tnf Α

Abstract Objective To investigate the expression of miR-195 and its target gene Bcl-2 in intervertebral disc degeneration (IVDD) and its effect on nucleus pulposus (NP) cell apoptosis. Methods The expressions of miR-195 and Bcl-2 in NP tissues of IVDD patients were quantified by qRT-PCR and western blotting, respectively. NP cells were divided into blank group, TNF-α group, TNF-α + miR-NC group, TNF-α + siBcl-2 group, and TNF-α + miR-195 inhibitors + siBcl-2 group. Cell proliferation was detected by MTT assay, cell apoptosis evaluated by flow cytometry, and mitochondrial membrane potential (MMP) tested by JC-1 staining. Moreover, the function of miR-195 on IVDD in vivo was investigated using a puncture-induced IVDD rat model. Results IVDD patients had significantly increased miR-195 expression and decreased Bcl-2 protein expression in NP tissues. The expression of miR-195 was negatively correlated with the expression of Bcl-2 in IVDD patients. Dual-luciferase reporter gene assay indicated that Bcl-2 was a target gene of miR-195. In comparison with blank group, TNF-α group showed decreased cell proliferation and MMP, increased cell apoptosis, upregulated expression of miR-195, Bax, and cleaved caspase 3, and downregulated Bcl-2 protein, while these changes were attenuated by miR-195 inhibitors. Additionally, siBcl-2 can reverse the protective effect of miR-195 inhibitors on TNF-α-induced NP cells. Besides, inhibition of miR-195 alleviated IVDD degeneration and NP cell apoptosis in the rat model. Conclusion MiR-195 was significantly upregulated in NP tissues of IVDD patients, and inhibition of miR-195 could protect human NP cells from TNF-α-induced apoptosis via upregulation of Bcl-2.

scholarly journals Pathomechanism of Insulin Resistance in Men with Central Obesity: Correlation of GGT, GPx, hs-CRP and Plasma Total Cysteine

2013 ◽  
Vol 5 (2) ◽  
pp. 101 ◽  
Author(s):  
Ritawaty Ritawaty ◽  
Indriyanti Rafi Sukmawati ◽  
Ilhamjaya Patellongi ◽  
Ferry Sandra
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Amino Acid ◽  
Fatty Liver ◽  
Central Obesity ◽  
Group Iv ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
Hs Crp

BACKGROUND: Gamma glutamyltransferase (GGT) was reported recently to be associated with inflammation, oxidative stress and increased amino acid. However, role of GGT in insulin resistance pathomechanism is not exactly known. Therefore correlation of GGT with inflammation, oxidative stress and elevated amino acid, in men with central obesity need to be confirmed.METHODS: A cross-sectional study was designed. Men with central obesity were recruited and selected. Anthropometric parameters, creatinine, hs-CRP, fasting glucose, fasting insulin, glutathione peroxidase (GPx) activity, GGT, plasma total cysteine (tCys) and fatty liver were measured. Subjects were then divided in 4 groups based on waist circumference (WC) and fatty liver: Group I: WC ≤100 cm, without fatty liver; Group II: WC ≤100 cm, with fatty liver; Group III: WC >100 cm, without fatty liver; Group IV: WC >100 cm, with fatty liver. All biochemical characteristics in each group were then statistically analyzed.RESULTS: Seventy-two men with central obesity were selected. Numbers of subjects in each group were: Group I: n=33; Group II: n=5; Group III: n=17; Group IV: n=17. We found significant difference of HOMA-IR between Group I and IV, significant correlation between GGT and HOMAIR, and significant negative correlation between tCys with HOMA-IR in Group IV.CONCLUSION: GGT was significantly correlated with HOMA-IR in men with WC >100 cm and fatty liver. Further investigation with more subjects is necessary to determine clear GGT cut-off to distinguish subjects with fatty liver and insulin resistance.KEYWORDS: GGT, hs-CRP, GPx, tCys, HOMA-IR, insulin resistance

Hsp22 Inhibits Oxidative Stress-Induced Endplate Chondrocyte Apoptosis by Regulating Mitochondrial Pathway

2021 ◽  
Vol 11 (10) ◽  
pp. 1947-1954
Author(s):  
Yi Ye ◽  
Xucan Wang ◽  
Zhenqing Yang ◽  
Qian Xu ◽  
Bo Zhang
Keyword(s):  
Oxidative Stress ◽  
Cell Apoptosis ◽  
Facet Joint ◽  
Mitochondrial Pathway ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ros Generation ◽  
Atp Level ◽  
Facet Joint Degeneration ◽  
Cyt C

Background: Facet joint degeneration (FJD), which is also called facet joint syndrome (FJS), has become one of the most commonly seen etiological factors for lumbago. Cartilage lesion triggered by lumbar facet joint (LFJ) degeneration might be related to mitochondrial impairment, but the its underlying mechanism remains unclear. Materials and methods: The endplate chondrocytes were induced by hydrogen peroxide (H2O2) to mimic the pathological conditions of oxidative stress. Enzyme linked immunosorbent assay (ELISA) were used for the evaluation of reactive oxygen species (ROS). Adenosine-triphosphate (ATP) level was assessed using ATP detection, along with the detection the expression of cytochrome C in mitochondria (mito-cyt c) and in cell cytoplasm (cyto-cyt c) and cleaved caspase 3 by Western blot analysis. TUNEL assay was conducted for the measurement of cell apoptosis in endplate chondrocytes. Reverse transcription-polymerase chain reaction (RT-qPCR) was used to verify the expression of heat shock protein 22 (HSP22) and the transfection efficiency of HSP22 interference plasmid. Results: It was found that H2O2 promoted the mitochondrial dysfunction, ROS generation and cell apoptosis in endplate chondrocytes. Moreover, HSP22 was down-regulated in H2O2-induced endplate chondrocytes, and interference of HSP22 decreased the ROS production, increased the ATP level and promoted the cell apoptosis, resulting in the enhanced impairment of endplate chondrocytes. Additionally, mitochondrial ROS inhibitor (Mito-TEMPO) ameliorated the injury effects of HSP22 silencing in the H2O2-induced endplate chondrocytes. Conclusion: In conclusion, HSP22 inhibits oxidative stress-induced endplate chondrocyte apoptosis by regulating mitochondrial pathway, possibly providing novel guidance direction for the treatment of LFJ degeneration.

scholarly journals Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C

Biomedicines ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 39
Author(s):  
Sahar Youssef ◽  
Marwa Salah
Keyword(s):  
Body Weight ◽  
Vitamin C ◽  
Adult Male ◽  
Control Group ◽  
Albino Rats ◽  
White Pulp ◽  
Group Iii ◽  
Group I ◽  
Tnf Α ◽  
Group Ii

Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.

scholarly journals Influence of Clarithromycin on Early Atherosclerotic Lesions after Chlamydia pneumoniae Infection in a Rabbit Model

2002 ◽  
Vol 46 (8) ◽  
pp. 2321-2326 ◽  
Author(s):  
Ignatius W. Fong ◽  
Brian Chiu ◽  
Esther Viira ◽  
Dan Jang ◽  
James B. Mahony
Keyword(s):  
Early Treatment ◽  
Chlamydia Pneumoniae ◽  
Rabbit Model ◽  
Treated Group ◽  
Group Iii ◽  
Delayed Treatment ◽  
Early Lesions ◽  
Atherosclerotic Lesions ◽  
Group I ◽  
Group Ii

ABSTRACT Chlamydia pneumoniae may play a role in atherogenesis and vascular diseases, and antibiotics may prove useful in these conditions. Three groups of New Zealand White rabbits (24 per group) were infected via the nasopharynx with C. pneumoniae on three separate occasions (2 weeks apart). Group I was untreated and sacrificed at 12 weeks; group II received clarithromycin at 20 mg/kg/day for 8 days, beginning 5 days after each inoculation (early treatment); and group III received a similar dose of clarithromycin starting 2 weeks after the third inoculation and continued for 6 weeks thereafter (delayed treatment). To test for a possible anti-inflammatory effect of clarithromycin, two other groups of uninfected rabbits (12 animals in each) were fed 0.5% cholesterol-enriched chow, and one of these groups was treated with clarithromycin at 30 mg/kg/day for 6 weeks. Of 23 untreated infected rabbits, 8 developed early lesions of atherosclerosis, whereas 2 of the 24 early-treated group II had similar changes (P = 0.036 [75% efficacy]). However, in the delayed-treatment group, group III, 3 of 24 rabbits developed early lesions of atherosclerosis, thus demonstrating 62.5% reduction compared to the untreated controls (P = 0.07 [trend to statistical significance]). C. pneumoniae antigen was detected in 8 of 23 group I (untreated) rabbits versus 1 of 24 of the early-treated (group II) rabbits and 4 of 24 animals in the delayed group III (P = 0.009 and 0.138, respectively). All of the untreated, cholesterol-fed rabbits had moderate to advanced atherosclerosis (grade III or IV); clarithromycin had no effect on reducing the prevalence of but did reduce the extent of atherosclerosis in the cholesterol-fed rabbits by 17% compared to untreated controls. Thus, clarithromycin administration modified C. pneumoniae-induced atherosclerotic lesions and reduced the ability to detect organism in tissue. Early treatment was more effective than delayed treatment.

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