RESUMEN

INTRODUCTION: Ginsenosides (GS) derived from Panax ginseng can regulate protein acetylation to promote mitochondrial function for protecting cardiomyocytes. However, the potential mechanisms of GS for regulating acetylation modification are not yet clear. OBJECTIVES: This study aimed to explore the potential mechanisms of GS in regulating protein acetylation and identify ginsenoside monomer for fighting myocardial ischemia-related diseases. METHODS: The 4D-lable free acetylomic analysis was employed to gain the acetylated proteins regulated by GS pretreatment. The co-immunoprecipitation assay, immunofluorescent staining, and mitochondrial respiration measurement were performed to detect the effect of GS or ginsenoside monomer on acetylated protein level and mitochondrial function. RNA sequencing, site-specific mutation, and shRNA interference were used to explore the downstream targets of acetylation modificationby GS. Cellular thermal shift assay and surface plasmon resonance were used for identifying the binding of ginsenoside with target protein. RESULTS: In the cardiomyocytes of normal, oxygen glucose deprivation and/or reperfusion conditions, the acetylomic analysis identified that the acetylated levels of spliceosome proteins were inhibited by GS pretreatment and SF3A2 acetylation at lysine 10 (K10) was significantly decreased as a potential target of GS. Ginsenoside Rb2 was identified as one of the active ginsenoside monomers for reducing the acetylation of SF3A2 (K10), which enhanced mitochondrial respiration against myocardial ischemic injury in in vivo and in vitro experiments. RNA-seq analysis showed that ginsenoside Rb2 promoted alternative splicing of mitochondrial function-related genes and the level of fascin actin-bundling protein 1 (Fscn1) was obviously upregulated, which was dependent on SF3A2 acetylation. Critically, thermodynamic, kinetic and enzymatic experiments demonstrated that ginsenoside Rb2 directly interacted with p300 for inhibiting its activity. CONCLUSION: These findings provide a novel mechanism underlying cardiomyocyte protection of ginsenoside Rb2 by inhibiting p300-mediated SF3A2 acteylation for promoting Fscn1 expression, which might be a promising approach for the prevention and treatment of myocardial ischemic diseases.

RESUMEN

BACKGROUND: Nicotinamide adenine dinucleotide (NAD+) metabolism is involved in the entire physiopathological process and is critical to human health. Long-term imbalance in NAD+ homeostasis is associated with various diseases, including non-alcoholic fatty liver disease, diabetes mellitus, cardiovascular diseases, neurodegenerative disorders, aging, and cancer, making it a potential target for effective therapeutic strategies. Currently, several natural products that target NAD+ metabolism have been widely reported to have significant therapeutic effects, but systematic summaries are lacking. PURPOSE: To summarize the latest findings on the prevention and treatment of various diseases through the regulation of NAD+ metabolism by various natural products in vivo and in vitro models, and evaluate the toxicities of the natural products. METHODS: PubMed, Web of Science, and ScienceDirect were searched using the keywords "natural products sources," "toxicology," "NAD+ clinical trials," and "NAD+," and/or paired with "natural products" and "diseases" for studies published within the last decade until January 2023. RESULTS: We found that the natural products mainly include phenols (curcumin, cyclocurcumin, 4-hydroxybenzyl alcohol, salvianolic acid B, pterostilbene, EGCG), flavonoids (pinostrobin, apigenin, acacetin, tilianin, kaempferol, quercetin, isoliquiritigenin, luteolin, silybin, hydroxysafflor yellow A, scutellarin), glycosides (salidroside), quinones (emodin, embelin, ß-LAPachone, shikonin), terpenoids (notoginsenoside R1, ginsenoside F2, ginsenoside Rd, ginsenoside Rb1, ginsenoside Rg3, thymoquinone, genipin), pyrazines (tetramethylpyrazine), alkaloids (evodiamine, berberine), and phenylpropanoids (ferulic acid). These natural products have antioxidant, energy-producing, anti-inflammatory, anti-apoptotic and anti-aging effects, which mainly influence the NAMPT/NAD+/SIRT, AMPK/SIRT1/PGC-1α, Nrf2/HO-1, PKCs/PARPs/NF-κB, and AMPK/Nrf2/mTOR signaling pathways, thereby regulating NAD+ metabolism to prevent and treat various diseases. These natural products have been shown to be safe, tolerable and have fewer adverse effects in various in vivo and in vitro studies and clinical trials. CONCLUSION: We evaluated the toxic effects of natural products and summarized the available clinical trials on NAD+ metabolism, as well as the recent advances in the therapeutic application of natural products targeting NAD+ metabolism, with the aim to provide new insights into the treatment of multiple disorders.

Asunto(s)

Productos Biológicos , Humanos , Animales , NAD/metabolismo , Productos Biológicos/farmacología , Productos Biológicos/uso terapéutico , Enfermedades Neurodegenerativas/tratamiento farmacológico , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Cardiovasculares/tratamiento farmacológico , Enfermedades Cardiovasculares/metabolismo , Diabetes Mellitus/tratamiento farmacológico , Diabetes Mellitus/metabolismo , Neoplasias/tratamiento farmacológico , Neoplasias/metabolismo

RESUMEN

ETHNOPHARMACOLOGICAL RELEVANCE: Metabolic syndrome (MetS) is a cluster of disease centered on obesity, which is the result of stagnation of liver qi according to traditional Chinese medicine. Panax notoginseng is a traditional Chinese herbal medicine, entering liver and stomach meridians and dissipating blood stasis, in which panax notoginseng saponins (PNS) are the main active components. However, its effects and mechanism on metabolic syndrome has not been revealed yet. AIM OF STUDY: To evaluate the anti-MetS effect of PNS, including body weight and adiposity, glucose metabolism and non-alcoholic fatty liver disease (NAFLD), as well as to explore the mechanism and signaling pathway of PNS on MetS effect. MATERIALS AND METHODS: HPLC was utilized to affirm the percentages of saponins in PNS. In vivo, normal C57BL/6J mice and high-fat diet (HFD)-induced MetS mice were used to evaluate anti-MetS effect of PNS. Body weight, food and water intake were recorded. NMR imager was used for NMR imaging and lipid-water analysis. Blood glucose detection, glucose and insulin tolerance test were performed to evaluate glucose metabolism. Biochemical indexes analysis and histopathological staining were used to evaluate the effect on NAFLD. The expressions of mRNA and proteins related to thermogenesis in adipose tissue were determined using real-time PCR and Western blot. In silico, network pharmacology was utilized to predict potential mechanism. In vitro, matured 3T3-L1 adipocyte was used as subject to confirm the signaling pathway by Western blot. RESULTS: We determined the content of PNS component by HPLC. In vivo, PNS could improve metabolic syndrome with weight loss, reduction of adiposity, improvement of adipose distribution, correction of glucose metabolism disorder and attenuation of NAFLD. Mechanismly, PNS boosted energy exhaustion and dramatically enhanced thermogenesis in brown adipose tissue (BAT), induced white adipose tissue (WAT) browning. In silico, utilizing network pharmacology strategy, we identified 307 candidate targets which were enriched in MAPK signaling pathway specifically in liver tissue and adipocyte. In vitro validation confirmed ERK and p38MAPK mediated anti-MetS effects of PNS, not JNK signaling pathway. CONCLUSION: PNS exerted protective effect on metabolic syndrome through MAPK-mediated adipose thermogenic activation, which may serve as a prospective therapeutic drug for metabolic syndrome.

Asunto(s)

Medicamentos Herbarios Chinos , Insulinas , Síndrome Metabólico , Enfermedad del Hígado Graso no Alcohólico , Panax notoginseng , Saponinas , Animales , Glucemia , Peso Corporal , Medicamentos Herbarios Chinos/farmacología , Glucosa , Lípidos , Síndrome Metabólico/tratamiento farmacológico , Ratones , Ratones Endogámicos C57BL , Farmacología en Red , Enfermedad del Hígado Graso no Alcohólico/tratamiento farmacológico , Obesidad/tratamiento farmacológico , Panax notoginseng/química , ARN Mensajero/metabolismo , Saponinas/farmacología , Saponinas/uso terapéutico , Agua

RESUMEN

BACKGROUND: Respiratory diseases mainly include asthma, influenza, pneumonia, chronic obstructive pulmonary disease, pulmonary hypertension, lung fibrosis, and lung cancer. Given their high prevalence and poor prognosis, the prevention and treatment of respiratory diseases are increasingly essential. In particular, the development for the novel strategies of drug treatment has been a hot topic in the research field. Ginsenosides are the major component of Panax ginseng C. A. Meyer (ginseng), a food homology and well-known medicinal herb. In this review, we summarize the current therapeutic effects and molecular mechanisms of ginsenosides in respiratory diseases. METHODS: The reviewed studies were retrieved via a thorough analysis of numerous articles using electronic search tools including Sci-Finder, ScienceDirect, PubMed, and Web of Science. The following keywords were used for the online search: ginsenosides, asthma, influenza, pneumonia, chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH), lung fibrosis, lung cancer, and clinical trials. We summarized the findings and the conclusions from 176 manuscripts on ginsenosides, including research articles and reviews. RESULTS: Ginsenosides Rb1, Rg1, Rg3, Rh2, and CK, which are the most commonly reported ginsenosides for treating of respiratory diseases, and other ginsenosides such as Rh1, Rk1, Rg5, Rd and Re, all primarily reduce pneumonia, fibrosis, and inhibit tumor progression by targeting NF-κB, TGF-ß/Smad, PI3K/AKT/mTOR, and JNK pathways, thereby ameliorating respiratory diseases. CONCLUSION: This review provides novel ideas and important aspects for the future research of ginsenosides for treating respiratory diseases.

Asunto(s)

Asma , Ginsenósidos , Hipertensión Pulmonar , Gripe Humana , Neoplasias Pulmonares , Panax , Enfermedad Pulmonar Obstructiva Crónica , Fibrosis Pulmonar , Humanos , Ginsenósidos/farmacología , Ginsenósidos/uso terapéutico , Ginsenósidos/química , Fibrosis Pulmonar/tratamiento farmacológico , Hipertensión Pulmonar/tratamiento farmacológico , Gripe Humana/tratamiento farmacológico , Fosfatidilinositol 3-Quinasas , Enfermedad Pulmonar Obstructiva Crónica/tratamiento farmacológico , Asma/tratamiento farmacológico , Neoplasias Pulmonares/tratamiento farmacológico , Panax/química

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Hemorrhagic shock (HS) is a shock result of hypovolemic injury, in which the innate immune response plays a central role in the pathophysiology ofthe severe complications and organ injury in surviving patients. During the development of HS, innate immunity acts as the first line of defense, mediating a rapid response to pathogens or danger signals through pattern recognition receptors. The early and exaggerated activation of innate immunity, which is widespread in patients with HS, results in systemic inflammation, cytokine storm, and excessive activation of complement factors and innate immune cells, comprised of type II innate lymphoid cells, CD4+ T cells, natural killer cells, eosinophils, basophils, macrophages, neutrophils, and dendritic cells. Recently, compelling evidence focusing on the innate immune regulation in preclinical and clinical studies promises new treatment avenues to reverse or minimize HS-induced tissue injury, organ dysfunction, and ultimately mortality. In this review, we first discuss the innate immune response involved in HS injury, and then systematically detail the cutting-edge therapeutic strategies in the past decade regarding the innate immune regulation in this field; these strategies include the use of mesenchymal stem cells, exosomes, genetic approaches, antibody therapy, small molecule inhibitors, natural medicine, mesenteric lymph drainage, vagus nerve stimulation, hormones, glycoproteins, and others. We also reviewed the available clinical studies on immune regulation for treating HS and assessed the potential of immune regulation concerning a translation from basic research to clinical practice. Combining therapeutic strategies with an improved understanding of how the innate immune system responds to HS could help to identify and develop targeted therapeutic modalities that mitigate severe organ dysfunction, improve patient outcomes, and reduce mortality due to HS injury.

Asunto(s)

Inmunidad Innata , Choque Hemorrágico , Humanos , Inmunoterapia , Células Asesinas Naturales , Insuficiencia Multiorgánica , Choque Hemorrágico/terapia

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Diverse pathogen effectors convergently target conserved components in plant immunity guarded by intracellular nucleotide-binding domain leucine-rich repeat receptors (NLRs) and activate effector-triggered immunity (ETI), often causing cell death. Little is known of the differences underlying ETI in different plants triggered by the same effector. In this study, we demonstrated that effector RipAW triggers ETI on Nicotiana benthamiana and Nicotiana tabacum. Both the first 107 amino acids (N1-107 ) and RipAW E3-ligase activity are required but not sufficient for triggering ETI on N. benthamiana. However, on N. tabacum, the N1-107 fragment is essential and sufficient for inducing cell death. The first 60 amino acids of the protein are not essential for RipAW-triggered cell death on either N. benthamiana or N. tabacum. Furthermore, simultaneous mutation of both R75 and R78 disrupts RipAW-triggered ETI on N. tabacum, but not on N. benthamiana. In addition, N. tabacum recognizes more RipAW orthologs than N. benthamiana. These data showcase the commonalities and specificities of RipAW-activated ETI in two evolutionally related species, suggesting Nicotiana species have acquired different abilities to perceive RipAW and activate plant defences during plant-pathogen co-evolution.

Asunto(s)

Ralstonia solanacearum , Epítopos , Enfermedades de las Plantas , Inmunidad de la Planta/genética , Dominios Proteicos , Nicotiana

RESUMEN

Cellular senescence is one of the most significant factors involved in aging and age-related diseases. Senescence of vascular smooth muscle cells (VSMCs) adversely affects the function of the cardiovascular system and contributes to the development of atherosclerosis, hypertension, and other cardiovascular diseases. Glucagon-like peptide-1 (GLP-1) is an important incretin hormone involved in insulin release and vascular tone. GLP-1 is quickly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). Omarigliptin is a new DPP-4 inhibitor that has demonstrated anti-inflammatory and antioxidative stress properties. In the present study, we investigated the effects of the selective DPP-4 inhibitor omarigliptin (OMG) on VSMCs exposed to insult from tumor necrosis factor-α (TNF-α), one of the main inflammatory signaling molecules involved in cellular senescence. We found that OMG could suppress TNF-α-induced expression of pro-inflammatory cytokines (interleukin-1ß (IL-1ß), IL-6, and IL-8) and inhibit oxidative stress by reducing the production of H2O2 and protein carbonyl. OMG ameliorated the increase in senescence-associated ß-galactosidase (SA-ß-gal) and telomerase activity induced by TNF-α. The plasminogen activator inhibitor-1 (PAI-1)/p53/p21 pathway is a key inducer of cellular senescence. OMG ameliorated the acetylation of p53 at lysine 382 (K382) and subsequent activation of p21 via inhibition of PAI-1. Importantly, our experiments revealed that blockage of silent information-regulator 1 (SIRT1) abolished the inhibitory effects of OMG on p53 acetylation, SA-ß-gal activity, and telomerase activity in VSMCs. These results suggest that OMG may have the potential to delay or prevent the progression of age-related cardiovascular diseases by modulating the activity of SIRT1.

Asunto(s)

Cardiotónicos/farmacología , Senescencia Celular/efectos de los fármacos , Inhibidores de la Dipeptidil-Peptidasa IV/farmacología , Compuestos Heterocíclicos con 2 Anillos/farmacología , Miocitos del Músculo Liso/efectos de los fármacos , Piranos/farmacología , Factor de Necrosis Tumoral alfa/farmacología , Animales , Aorta/citología , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/metabolismo , Inflamación/prevención & control , Masculino , Músculo Liso Vascular/citología , Estrés Oxidativo/efectos de los fármacos , Inhibidor 1 de Activador Plasminogénico/metabolismo , Ratas Sprague-Dawley , Inhibidores de Serina Proteinasa/farmacología , Sirtuina 1/metabolismo , Proteína p53 Supresora de Tumor/metabolismo

RESUMEN

Once protein synthesis is excessive or misfolded protein becomes aggregated, which eventually overwhelms the capacity of the endoplasmic reticulum (ER), a state named ER stress would be reached. ER stress could affect many tissues, especially the liver, in which nonalcoholic fatty liver disease, liver steatosis, etc. have been reported relative. However, there is still a lack of systematic insight into ER stress in the liver, which can be obtained by integrating metabolomics and transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. Microarray and untargeted metabolomics were performed to identify the genes and metabolites significantly altered in liver tissues. Surprisingly, apart from the predictable unfolded protein response, liver lipid, arginine, and proline metabolisms were affirmed to be related to ER stress. Also, the ketone body metabolism changed most prominently in response to ER stress, with few studies backing. What is more, succinate receptor 1 (Sucnr1) may be a novel marker and therapeutical target of liver ER stress. In this study, the combination of the metabolome and transcriptome provided reliable information about liver pathological processes, including key relative pathways, potential markers, and targets involved in ER stress of the liver.

Asunto(s)

Metabolismo de los Lípidos , Enfermedad del Hígado Graso no Alcohólico , Animales , Estrés del Retículo Endoplásmico/genética , Cetonas , Metabolismo de los Lípidos/genética , Hígado/metabolismo , Metabolómica , Ratones , Ratones Endogámicos C57BL , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Transcriptoma

RESUMEN

Endoplasmic reticulum (ER) stress is a cellular state that results from the overload of unfolded/misfolded protein in the ER that, if not resolved properly, can lead to cell death. Both acute lung infections and chronic lung diseases have been found related to ER stress. Yet no study has been presented integrating metabolomic and transcriptomic data from total lung in interpreting the pathogenic state of ER stress. Total mouse lungs were used to perform LC-MS and RNA sequencing in relevance to ER stress. Untargeted metabolomics revealed 16 metabolites of aberrant levels with statistical significance while transcriptomics revealed 1593 genes abnormally expressed. Enrichment results demonstrated the injury ER stress inflicted upon lung through the alteration of multiple critical pathways involving energy expenditure, signal transduction, and redox homeostasis. Ultimately, we have presented p-cresol sulfate (PCS) and trimethylamine N-oxide (TMAO) as two potential ER stress biomarkers. Glutathione metabolism stood out in both omics as a notably altered pathway that believed to take important roles in maintaining the redox homeostasis in the cells critical for the development and relief of ER stress, in consistence with the existing reports.

Asunto(s)

Cresoles/metabolismo , Estrés del Retículo Endoplásmico/fisiología , Glutatión/metabolismo , Lesión Pulmonar/diagnóstico , Metilaminas/metabolismo , Ésteres del Ácido Sulfúrico/metabolismo , Animales , Biomarcadores/análisis , Biomarcadores/metabolismo , Cresoles/análisis , Estrés del Retículo Endoplásmico/genética , Perfilación de la Expresión Génica/métodos , Pulmón/química , Pulmón/metabolismo , Pulmón/patología , Lesión Pulmonar/genética , Lesión Pulmonar/metabolismo , Lesión Pulmonar/patología , Masculino , Metabolómica/métodos , Metilaminas/análisis , Ratones , Ratones Endogámicos C57BL , Estrés Oxidativo/genética , Estrés Oxidativo/fisiología , Ésteres del Ácido Sulfúrico/análisis , Respuesta de Proteína Desplegada/genética , Respuesta de Proteína Desplegada/fisiología

RESUMEN

Alternative splicing (AS) is an important mechanism by which eukaryotes regulate transcription and protein diversity. The dynamic changes in AS that occur on a genome-wide scale during interactions between plant roots and pathogens remain unknown. Here, we used the interaction between Arabidopsis and Ralstonia solanacearum as a model to explore the AS changes that take place during the response of roots to infection by means of high-throughput RNA-sequencing. We showed that dynamic changes in AS occur much earlier than changes at the level of transcription during R.solanacearum infection. Comparing genes that are regulated at the transcriptional and AS levels indicated that there are few common genes between differentially spliced genes (DSGs) and differentially expressed genes (DEGs). The functional gene ontology (GO) analysis identified that the enriched GO terms for the DSGs were different from those of the DEGs. The DSGs were over-represented in GO terms associated with post-transcriptional and translational regulations, suggesting that AS may act on RNA stability and during post-translation, thus affecting the output of plant defense molecules. Meanwhile, changes in DSGs were infection stage-specific. Furthermore, the nucleotide binding domain and leucine-rich repeat proteins and receptor-like kinases, key regulators in plant immunity, were shown to undergo dynamic changes in AS in response to R. solanacearum. Taken together, AS, along with transcription, modulates plant root defense to R. solanacearum through transcriptome reprogramming.

Asunto(s)

Empalme Alternativo , Proteínas de Arabidopsis/genética , Arabidopsis/genética , Enfermedades de las Plantas/genética , Raíces de Plantas/genética , Ralstonia solanacearum/fisiología , Transcriptoma , Arabidopsis/microbiología , Regulación de la Expresión Génica de las Plantas , Secuenciación de Nucleótidos de Alto Rendimiento , Enfermedades de las Plantas/microbiología , Raíces de Plantas/microbiología

RESUMEN

Objective: To evaluate whether or not highly active antiretroviral therapy is associated with carotid artery stiffness in human immunodeficiency virus-positive patients in Henan Province, China. Method: Fifty human immunodeficiency virus-positive patients with at least a 5-year history of highly active antiretroviral therapy use and 50 human immunodeficiency virus-positive patients without a history of highly active antiretroviral therapy use were enrolled in this study. Carotid artery intima-media thickness and stiffness were determined by quantitative inter-media thickness and quantitative artery stiffness, respectively. Results: No statistically significant difference in carotid artery intima-media thickness and stiffness was observed between groups. A significant association between human immunodeficiency virus infection time and carotid artery stiffness was observed, but no significant association between human immunodeficiency virus infection time and intima-media thickness was found. No significant association between intima-media thickness, stiffness, and CD4+ and CD8+ T-cell counts were observed. Conclusion: The first-line highly active antiretroviral therapy currently used in China is not associated with carotid artery stiffness in human immunodeficiency virus-positive patients with good highly active antiretroviral therapy compliance. Human immunodeficiency virus may play a role in the development of atherosclerosis. .

Asunto(s)

Femenino , Humanos , Masculino , Persona de Mediana Edad , Terapia Antirretroviral Altamente Activa/efectos adversos , Aterosclerosis/inducido químicamente , Grosor Intima-Media Carotídeo , Arterias Carótidas/efectos de los fármacos , Infecciones por VIH/tratamiento farmacológico , Rigidez Vascular , Estudios Transversales , Arterias Carótidas/fisiopatología , Factores de Tiempo , Carga Viral

RESUMEN

OBJECTIVE: To evaluate whether or not highly active antiretroviral therapy is associated with carotid artery stiffness in human immunodeficiency virus-positive patients in Henan Province, China. METHOD: Fifty human immunodeficiency virus-positive patients with at least a 5-year history of highly active antiretroviral therapy use and 50 human immunodeficiency virus-positive patients without a history of highly active antiretroviral therapy use were enrolled in this study. Carotid artery intima-media thickness and stiffness were determined by quantitative inter-media thickness and quantitative artery stiffness, respectively. RESULTS: No statistically significant difference in carotid artery intima-media thickness and stiffness was observed between groups. A significant association between human immunodeficiency virus infection time and carotid artery stiffness was observed, but no significant association between human immunodeficiency virus infection time and intima-media thickness was found. No significant association between intima-media thickness, stiffness, and CD4(+) and CD8(+) T-cell counts were observed. CONCLUSION: The first-line highly active antiretroviral therapy currently used in China is not associated with carotid artery stiffness in human immunodeficiency virus-positive patients with good highly active antiretroviral therapy compliance. Human immunodeficiency virus may play a role in the development of atherosclerosis.

Asunto(s)

Terapia Antirretroviral Altamente Activa/efectos adversos , Aterosclerosis/inducido químicamente , Arterias Carótidas/efectos de los fármacos , Grosor Intima-Media Carotídeo , Infecciones por VIH/tratamiento farmacológico , Rigidez Vascular , Recuento de Linfocito CD4 , Arterias Carótidas/fisiopatología , Estudios Transversales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores de Tiempo , Carga Viral

RESUMEN

Chronic heart disease contributes to the mortality of patients with AIDS. Although studies of left ventricular function in patients with acquired immune deficiency syndrome (AIDS) have been conducted, studies of right ventricular function are rare. The present study aimed to characterize the tricuspid annulus movement and evaluate the right ventricular function of patients with AIDS by tissue Doppler imaging. Tissue Doppler echocardiography was performed on 106 patients with AIDS and 64 controls. Tricuspid annulus movements were detected from the apical four-chamber view and the apical right heart two-chamber view. The peak diastolic early period velocity (Ve), peak diastolic later period velocity (Va) and peak systolic velocity (Vs) were measured at the anterior, posterior and lateral walls and also at the interventricular septum. Mean values were calculated, as well as the Tei index of the lateral site. Compared with the values in the control group, the Vs and Va of the AIDS group decreased at all sites with the exception of the lateral wall, whereas the Ve decreased at all sites of the tricuspid annulus (P<0.05). The Tei index was higher in the AIDS group than in the control (P<0.05). The results obtained in the present study show that the function of the right ventricle decreases in patients with AIDS, which is indicative of susceptibility to right ventricular dysfunction.