Genome-wide identification and molecular expression profile analysis of FHY3/FAR1 gene family in walnut (Juglans sigillata L.) development.

BACKGROUND: Juglans sigillata L. (walnut) has a high economic value for nuts and wood and has been widely grown and eaten around the world. Light plays an important role in regulating the development of the walnut embryo and promoting nucleolus enlargement, which is one of the factors affecting the yield and quality of walnut. However, little is known about the effect of light on the growth and quality of walnuts. Studies have shown that far red prolonged hypocotyl 3 (FHY3) and far red damaged response (FAR1) play important roles in plant growth, light response, and resistance. Therefore, FHY3/FAR1 genes were identified in walnuts on a genome-wide basis during their growth and development to reveal the potential regulation mechanisms involved in walnut kernel growth and development. RESULTS: In the present study, a total of 61 FHY3/FAR1 gene family members in walnuts have been identified, ranging in length from 117 aa to 895 aa. These gene family members have FHY3 or FAR1 conserved domains, which are unevenly distributed on the 15 chromosomes (Chr) of the walnut (except for the Chr16). All 61 FHY3/FAR1 genes were divided into five subclasses (I, II, III, IV, and V) by phylogenetic tree analysis. The results indicated that FHY3/FAR1 genes in the same subclasses with similar structures might be involved in regulating the growth and development of walnut. The gene expression profiles were analyzed in different walnut kernel varieties (Q, T, and F). The result showed that some FHY3/FAR1 genes might be involved in the regulation of walnut kernel ripening and seed coat color formation. Seven genes (OF07056-RA, OF09665-RA, OF24282-RA, OF26012-RA, OF28029-RA, OF28030-RA, and OF08124-RA) were predicted to be associated with flavonoid biosynthetic gene regulation cis-acting elements in promoter sequences. RT-PCR was used to verify the expression levels of candidate genes during the development and color change of walnut kernels. In addition, light responsiveness and MeJA responsiveness are important promoter regulatory elements in the FHY3/FAR1 gene family, which are potentially involved in the light response, growth, and development of walnut plants. CONCLUSION: The results of this study provide a valuable reference for supplementing the genomic sequencing results of walnut, and pave the way for further research on the FHY3/FAR1 gene function of walnut.

Hepatic Energy Metabolism under the Local Control of the Thyroid Hormone System.

The energy homeostasis of the organism is orchestrated by a complex interplay of energy substrate shuttling, breakdown, storage, and distribution. Many of these processes are interconnected via the liver. Thyroid hormones (TH) are well known to provide signals for the regulation of energy homeostasis through direct gene regulation via their nuclear receptors acting as transcription factors. In this comprehensive review, we summarize the effects of nutritional intervention like fasting and diets on the TH system. In parallel, we detail direct effects of TH in liver metabolic pathways with regards to glucose, lipid, and cholesterol metabolism. This overview on hepatic effects of TH provides the basis for understanding the complex regulatory network and its translational potential with regards to currently discussed treatment options of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) involving TH mimetics.

Lung cancer patients with chronic obstructive pulmonary disease benefit from anti-PD-1/PD-L1 therapy.

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) are two of the most fatal respiratory diseases, seriously threatening human health and imposing a heavy burden on families and society. Although COPD is a significant independent risk factor for LC, it is still unclear how COPD affects the prognosis of LC patients, especially when LC patients with COPD receive immunotherapy. With the development of immune checkpoint inhibition (ICI) therapy, an increasing number of inhibitors of programmed cell death-1 (PD-1) and PD-1 ligand (PD-L1) have been applied to the treatment of LC. Recent studies suggest that LC patients with COPD may benefit more from immunotherapy. In this review, we systematically summarized the outcomes of LC patients with COPD after anti-PD-1/PD-L1 treatment and discussed the tumor immune microenvironment (TIME) regulated by COPD in LC immunotherapy, which provides novel insights for the clinical treatment of LC patients with COPD.

Venovenous vs. Venoarterial Extracorporeal Membrane Oxygenation in Infection-Associated Severe Pediatric Acute Respiratory Distress Syndrome: A Prospective Multicenter Cohort Study.

Background: Extracorporeal membrane oxygenation (ECMO) has been increasingly used as rescue therapy for severe pediatric acute respiratory distress syndrome (PARDS) over the past decade. However, a contemporary comparison of venovenous (VV) and venoarterial (VA) ECMO in PARDS has yet to be well described. Therefore, the objective of our study was to assess the difference between VV and VA ECMO in efficacy and safety for infection-associated severe PARDS patients. Methods: This prospective multicenter cohort study included patients with infection-associated severe PARDS who received VV or VA ECMO in pediatric intensive care units (PICUs) of eight university hospitals in China between December 2018 to June 2021. The primary outcome was in-hospital mortality. Secondary outcomes included ECMO weaning rate, duration of ECMO and mechanical ventilation (MV), ECMO-related complications, and hospitalization costs. Results: A total of 94 patients with 26 (27.66%) VV ECMO and 68 (72.34%) VA ECMO were enrolled. Compared to the VA ECMO patients, VV ECMO patients displayed a significantly lower in-hospital mortality (50 vs. 26.92%, p = 0.044) and proportion of neurologic complications, shorter duration of ECMO and MV, but the rate of successfully weaned from ECMO, bleeding, bloodstream infection complications and pump failure were similar. By contrast, oxygenator failure was more frequent in patients receiving VV ECMO. No significant intergroup difference was observed for the hospitalization costs. Conclusion: These positive findings showed the conferred survival advantage and safety of VV ECMO compared with VA ECMO, suggesting that VV ECMO may be an effective initial treatment for patients with infection-associated severe PARDS.

Ethyl 2-Succinate-Anthraquinone Attenuates Inflammatory Response and Oxidative Stress via Regulating NLRP3 Signaling Pathway.

Aloe-emodin widely possesses antibacterial, anti-inflammatory, antioxidant, antiviral, and anti-infectious properties. This study investigated the effect of ethyl 2-succinate-anthraquinone (Luhui derivative, LHD) on inflammation. In vitro, a THP-1 macrophage inflammation model, made by 100 ng/ml phorbol-12-myristate-13-acetate (PMA) and 1 µg/ml LPS for 24 h, was constructed. The LHD group (6.25 µmol/L, 12.5 µmol/L, 25 µmol/L, 50 µmol/L) had no effect on THP-1 cell activity, and the expression of IL-6 mRNA was down-regulated in a concentration-dependent manner, of which the 25 µmol/L group had the best inhibitory effect. The migration of THP-1 macrophages induced by LPS was decreased by the LHD. Moreover, the LHD suppressed ROS fluorescence expression by inhibiting MDA expression and increasing SOD activity. In vivo, we revealed that the LHD, in different doses (6.25 mg/kg, 12.5 mg/kg, 25 mg/kg, 50 mg/kg), has a protective effect on stress physiological responses by assessing the body temperature of mice. Interestingly, acute lung injury (e.g., the structure of the alveoli disappeared and capillaries in the alveolar wall were dilated and congested) and liver damage (e.g., hepatocyte swelling, neutrophil infiltration, and hepatocyte apoptosis) were obviously improved at the same condition. Furthermore, we initially confirmed that the LHD can down-regulate the expression of NLRP3, IL-1ß, and caspase-1 proteins, thereby mediating the NLRP3 inflammasome signaling pathway to produce anti-inflammatory effects. In conclusion, our results indicate that the LHD exerts anti-inflammatory activity via regulating the NLRP3 signaling pathway, inhibition of oxidative stress, and THP-1 macrophage migration.

Effects of continuous venovenous hemofiltration on vancomycin trough concentrations in critically ill children.

BACKGROUND: Vancomycin trough concentrations are associated with clinical outcomes and drug adverse effects. This study investigates the effects of continuous venovenous hemofiltration (CVVH) on vancomycin trough concentrations in critically ill children with a vancomycin dosage of 40-60 mg/kg/day. METHODS: Children with steady-state vancomycin trough concentrations admitted to the pediatric intensive care unit (PICU) between January 2016 and December 2019 were retrospectively enrolled. Patients were divided into CVVH and non-CVVH groups according to treatment differences and renal function. Vancomycin trough concentrations were then compared between the groups, and risk factors for supratherapeutic trough concentrations (>20 mg/L) were analyzed with logistic regression. RESULTS: Of the 119 patients included, 35 were enrolled in the CVVH group and 84 in the non-CVVH group. Median vancomycin trough concentrations were significantly higher in the CVVH group than those in the non-CVVH group [14.9 (IQR =9.6-19.6) vs. 9.3 (IQR =7.0-13.4), P<0.001] and the proportion of therapeutic trough concentrations (10-20 mg/L) was similar between CVVH and non-CVVH groups (54.3% vs. 39.3%, P=0.133). However, CVVH therapy patients had a significantly higher proportion of supratherapeutic trough concentrations (20.0% vs. 1.2%, P=0.001) compared to the non-CVVH group. Multivariate analysis demonstrated that the Pediatric Risk of Mortality (PRISM) III score ≥28 (OR =13.7; 95% CI, 1.4-137.0; P=0.026] was an independent risk factor for supratherapeutic trough concentrations in critically ill patients. CONCLUSIONS: CVVH therapy affects vancomycin trough concentrations and is associated with supratherapeutic concentrations with a 40-60 mg/kg/day vancomycin dosage. PRISM III scores ≥28 may serve as an independent risk factor for supratherapeutic trough concentrations in children receiving CVVH therapy.

Aloe-emodin relieves zidovudine-induced injury in neonatal rat ventricular myocytes by regulating the p90rsk/p-bad/bcl-2 signaling pathway.

BACKGROUND/AIMS: Zidovudine (3'-azido-2',3'-deoxythymidine; AZT) is a first-line drug for treatment of human immunodeficiency virus infection (HIV). However, its application is limited by cardiotoxicity due to cardiomyocyte injury. This study investigated whether Aloe-emodin (AE), an anthraquinone compound, protects against AZT-induced cardiomyocyte toxicity. METHODS: MTT, JC-1 assays and TUNEL were examined to verify the protective effect of AE against AZT-induced cardiomyocyte injury. Western blotting was performed to explore the anti-apoptotic effect of AE using anti-apoptotic proteins p90rsk, p-bad, and bcl-2 and pro-apoptotic proteins apaf-1, cleaved-caspase-3, and cytochrome c. RESULTS: We observed a protective effect of AE against cell viability decrease and TUNEL positive cells increase induced by AZT, which was counteracted by BI-D1870. Western blot analysis found that AE significantly inhibited cardiomyocyte apoptosis by activating p90rsk/p-bad/bcl-2 signaling pathway. Furthermore, BI-D1870 counteracted the anti-apoptotic effect of AE. CONCLUSIONS: Taken together, these results indicate that AE attenuated AZT-induced cardiomyocyte apoptosis by activating p90rsk.

Vasculoprotective effects of Centella asiatica, Justicia gendarussa and Imperata cylindrica decoction via the NOXs-ROS-NF-κB pathway in spontaneously hypertensive rats.

BACKGROUND AND AIM: Centella asiatica, Justicia gendarussa and Imperata cylindrica decoction (CJID) is efficacious for hypertension. NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (NOX)-induced reactive oxygen species (ROS) generation modulates nuclear factor kappa B (NF-κB) activation and thus mediates hypertension-induced vascular remodeling. This research aims to investigate the anti-remodeling effect of CJID through the mechanism of NOXs-ROS-NF-κB pathway in spontaneously hypertensive rats (SHRs). EXPERIMENTAL PROCEDURE: CJID was orally administered once a day for five weeks in SHRs and normotensive-WKY (Wistar Kyoto) rats. All rats were sacrificed at the end of study and different assays were performed to determine whether CJID ameliorates vascular remodeling in SHRs, such as histological examination; lactate dehydrogenase (LDH), nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) assays; superoxide and hydrogen peroxide (H2O2) generation assays, immunohistochemistry and immunofluorescence assays. . Changes in levels of inducible nitric oxide synthase (iNOS), NF-κB-p65, NF-κB inhibitor alpha/IκBα (inhibitory kappa B- alpha), phosphorylation of IκBα (p-IκBα) and NOX1, NOX2, NOX4 in the thoracic aorta were determined. RESULTS: Vascular remodeling indicators, media thickness, collagen and elastic accumulation in the thoracic aorta, of SHRs-treated CJID were attenuated. Redox homeostasis, aortic superoxide and hydrogen peroxide generation were decreased in SHRs-treated group. Aortic iNOS, p-IκBα, NF-κB-p65 and NOX1, NOX2, NOX4 expressions were suppressed. CONCLUSIONS: CJI treatment diminishes oxidative stress response in the thoracic aorta of SHRs via regulation of NOXs-ROS-NF-κB signaling pathway. These findings indicate that CJI possess protective effect against hypertension-induced vascular remodeling in SHRs.

Bioinformatic identification of hub genes and key pathways in neutrophils of patients with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is characterized as a neutrophil-dominant disorder without effective pharmacological interventions. Knowledge of neutrophils in ARDS patients at the transcriptome level is still limited. We aimed to identify the hub genes and key pathways in neutrophils of patients with ARDS. The transcriptional profiles of neutrophils from ARDS patients and healthy volunteers were obtained from the GSE76293 dataset. The differentially expressed genes (DEGs) between ARDS and healthy samples were screened using the limma R package. Subsequently, functional and pathway enrichment analyses were performed based on the database for annotation, visualization, and integrated discovery (DAVID). The construction of a protein-protein interaction network was carried out using the search tool for the retrieval of interacting genes (STRING) database and the network was visualized by Cytoscape software. The Cytoscape plugins cytoHubba and MCODE were used to identify hub genes and significant modules. Finally, 136 upregulated genes and 95 downregulated genes were identified. Gene ontology analyses revealed MHC class II plays a major role in functional annotations. SLC11A1, ARG1, CHI3L1, HP, LCN2, and MMP8 were identified as hub genes, and they were all involved in the neutrophil degranulation pathway. The MAPK and neutrophil degranulation pathways in neutrophils were considered as key pathways in the pathogenesis of ARDS. This study improves our understanding of the biological characteristics of neutrophils and the mechanisms underlying ARDS, and key pathways and hub genes identified in this work can serve as targets for novel ARDS treatment strategies.

Retraction: The unanimity of fluid restriction is still debating in patients with heart failure.

The paper entitled "The unanimity of fluid restriction is still debating in patients with heart failure" by Chen et al., which was published online on April 21, 2020, has been withdrawn by the Publisher because it commented an article by Dr. De Vecchis et al. entitled "Effects of a restricted water intake on various clinical and laboratory outcomes in patients with heart failure: a meta-analysis of randomized controlled trials" which has been retracted due to self-plagiarism.

Aloe Emodin Reduces Cardiac Inflammation Induced by a High-Fat Diet through the TLR4 Signaling Pathway.

BACKGROUND: Aloe emodin (AE) is a lipid-lowering agent, which could be used to treat hyperlipidemia, thereby reducing the risk of cardiovascular disease. Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages. PURPOSE: The purpose of this study is to evaluate the potential roles and mechanisms of AE in hyperlipidemia-induced oxidative stress and inflammation in the heart. Study Design. We established a hyperlipidemia-induced cardiac inflammation model in rats and cells then administered AE and observed its effect on hyperlipidemia-induced cardiac inflammation. METHODS: We used a mouse model of hyperlipidemia caused by a high-fat diet (HFD) for 10 weeks and cell culture experimental models of inflammation in the heart stimulated by PA for 14 h. Inflammatory markers were detected by qRT-PCR, WB, and immunofluorescence. RESULTS: We demonstrated that the expression levels of proinflammatory cytokines IL-1ß, IL-6, and TNF-α were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. Our in vitro study showed AE treatment dose-dependently decreased the expression of IL-1ß, IL-6, and TNF-α were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. Our κB, and p-P65l in vivo and in vitro study showed AE treatment dose-dependently decreased the expression of IL-1. CONCLUSION: Taken together, our findings disclose that AE could alleviate HFD/PA-induced cardiac inflammation via inhibition of the TLR4/NF-κB signaling pathway. Thus, AE may be a promising therapeutic strategy for preventing hyperlipidemia-induced myocardial injury.κB, and p-P65l.

Ascending Aortic Aneurysm After Repair of Aortico-Left Ventricular Tunnel.

Ascending aortic aneurysm following aortico-left ventricular tunnel (ALVT) repair is an uncommon but life-threatening complication. A 27-year-old man had received patch closure for ALVT at infancy. Eighteen years later, aortic valve replacement for severe aortic regurgitation and direct suture for recurrent slit tunnel were performed. Another 9 years later, ascending aortic replacement was performed because of ascending aortic aneurysm. Thus we report an uncommon case of ascending aortic aneurysm 27 years after the repair of an ALVT.

A case report of a teenager with severe hand, foot, and mouth disease with brainstem encephalitis caused by enterovirus 71.

BACKGROUND: Hand, foot, and mouth disease (HFMD) is an acute viral infection occurring mostly in infants and children. Enterovirus 71 (EV71) infection mostly occurs in children < 5 years of age. Severe cases, however, are usually encountered in children under the age of 3 years, and exceedingly rare in teenagers > 14 years and adults. CASE PRESENTATION: We report a rare case of HFMD in a 16-year-old male teenager residing in Chonqing, China. The clinical presentation was typical of HFMD and included vesicular lesions and oral mucosal ulcers, macular and vesicular lesions on palms and soles. He developed severe neurological complications that were suggestive of brainstem encephalitis. EV71 RNA was detected in the patient's faecal samples by reverse transcription-polymerase chain reaction. Specific IgM antibody to EV71 was detected in both serum and cerebrospinal fluid by ELISA. Gamma immunoglobulin therapy at 25 g/day was administered for 2 days, along with methylprednisolone, mannitol, ganglioside, and creatine phosphate sodium. The patient showed neurological improvement and recovered completely in 1 month. CONCLUSIONS: This case indicates that EV71 infection may cause HFMD in teenagers with potentially severe neurological involvement. Clinicians should be aware of the possibility of HFMD occurring in adults and teenagers as prompt treatment could be life-saving in these patients.

Significance of preoperative acute kidney injury in patients with acute type A aortic dissection.

BACKGROUND/PURPOSE: Acute type A aortic dissection (AAD) is a medical emergency with high mortality even with emergency repair. We explored the risk factors for in-hospital mortality and the impact of preoperative acute kidney injury (AKI) in patients with AAD. METHODS: Our hospital database contained records for 156 consecutive patients who underwent AAD repair between March 2000 and February 2013. They were assigned to the in-hospital mortality or the survival group. All data were collected retrospectively. RESULTS: The 30-day mortality, including intraoperative deaths, was 14.1% (22/156). Total in-hospital mortality was 19.2% (30/156). Patients who required preoperative cardiopulmonary resuscitation (CPR) (16.7 vs 3.2%; P = 0.012), or who presented with preoperative cardiac tamponade (46.7 vs 19.0%; P = 0.002), shock/hypotension (56.7 vs 21.4%; P < 0.001), or coma (20.0 vs 6.3%; P = 0.019) had a higher in-hospital mortality rate. There was no difference in in-hospital mortality rate between patients with preoperative AKI or not. Mortality and major complications were significantly correlated with the severity of AKI. Multivariate analysis confirmed that preoperative shock or hypotension (odds ratio = 5.2; 95% CI = 2.2-12.3), and preoperative AKI stage 3 (odds ratio = 4.9; 95% CI = 1.3-19.3) were independent preoperative prognostic factors of in-hospital mortality. CONCLUSION: On the basis of our results, preoperative stage 3 AKI is a crucial prognostic risk factor for patients with AAD repair, Cardiac surgeons should be aware of this condition when dealing with AAD patients.

Activation of cardiac TrkB receptor by its small molecular agonist 7,8-dihydroxyflavone inhibits doxorubicin-induced cardiotoxicity via enhancing mitochondrial oxidative phosphorylation.

Brain-derived neurotrophic factor (BDNF)/tropomyosin-related receptor kinase B (TrkB) pathway has been revealed as a novel therapeutic target for several neurological diseases. Recently, small-molecule TrkB agonist 7,8-dihydroxyflavone (7,8-DHF) has received considerable attention as a novel potential candidate for the treatment of various BDNF-implicated human disorders. However, its roles in cardiac diseases are not fully understood. Here, the present study aimed to clarify the effects and mechanisms of 7,8-DHF on doxorubicin (Dox)-induced cardiotoxicity. Kunming mice and H9c2 cells were employed to investigate the functional role of 7,8-DHF both in vivo and in vitro. 7,8-DHF markedly increased cell viability and reduced cell death of Dox-treated cells. Meanwhile, 7,8-DHF significantly increased mitochondrial respiration, membrane potential, and optic atrophy 1 (OPA1) protein expression. 7,8-DHF improved cardiac function and attenuated cardiac injury in Dox mice model. Expression of AMP-activated protein kinase (AMPK) and signal transducers and activators of transcription 3 (STAT3) was restored by 7,8-DHF. Furthermore, the protective role of 7,8-DHF was abolished by ANA-12 (a specific antagonist of TrkB). In elucidating the molecular mechanism, the phosphorylation of Akt was significantly increased while extracellular regulated protein kinase (ERK) was decreased after 7,8-DHF treatment. The regulatory effects of 7,8-DHF on STAT3 and AMPK was reversed by Akt inhibitor. In summary, 7,8-DHF attenuated Dox-induced cardiotoxicity by activating Akt and increasing mitochondrial oxidative phosphorylation and thereby regulating STAT3, AMPK, and ERK signals. The present study enhanced current understanding of TrkB receptor in the cardiovascular system and provided a novel target for prevention and treatment of heart diseases.

Fate of distal aorta after acute type A aortic dissection repair: Change and persistency of postoperative false lumen status.

BACKGROUND: The role of false lumen patency related to aortic growth, re-interventions, and post-discharge mortality in the chronic phase of repaired type A acute aortic dissection (TAAAD) remains controversial. We investigated the role of postoperative false lumen patency during long-term follow-up. METHODS: Based on postoperative CT images of 70 candidates, 58 eligible patients without alteration of false lumen status were assigned into three groups: complete patency, partial patency, and complete thrombosis. Aortic growth of 7 levels was analyzed. RESULTS: Persistent complete patency in post-operative TAAAD presents faster expansion of aortic diameter (95% CI, 0.35 to 11.52; P=0.038; B=5.935) and more patients with growth rate>5mm/year (P=0.029). The persistent status of false lumen does not predict post-discharge mortality (P=0.479). History of coronary artery disease (CAD) is the only independent predictor of post-discharge mortality. CONCLUSIONS: In TAAAD patients without change of postoperative false lumen status, completely patent false lumen presents faster aortic growth and more patients with growth rate>5mm/year. False lumen status does not correlate with late survival. Here we provide an insight into persistent postoperative false lumen in TAAAD patients and may help cast light on aortic dissection in this specific subgroup to improve their late outcomes.

Indonesian herbal medicine prevents hypertension-induced left ventricular hypertrophy by diminishing NADPH oxidase-dependent oxidative stress.

Indonesian herbal medicine Centella asiatica, Justicia gendarussa and Imperata cylindrica decoction (CJID) are known to be efficacious for hypertension. Oxidative stress plays an important role in hypertension-induced left ventricular hypertrophy (H-LVH). This study evaluated whether CJID inhibit cardiac remodeling in spontaneously hypertensive rats (SHRs) through mechanism of oxidative stress-related cardiac-NADPH oxidase (NOXs) pathway: NOX1, NOX2 and NOX4. Forty-weeks-old SHRs and normotensive-WKY rats, were both randomly divided into 2 groups: CJID and control. All rats were treated for 5 weeks. Systolic blood pressure (SBP) and heart rate (HR) were measured. LV morphology, function and performance were assessed by histological staining and echocardiography. Serum and cardiac superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assessed. Cardiac superoxide and hydrogen peroxide (H2O2) productions, protein expressions of SOD2, SOD3, NOX1, NOX2 and NOX4 were also determined. We found that SBP and HR were significantly decreased in SHRs-treated group. Echocardiography showed that CJID significantly improved LV morphometry and function. CJID decreased MDA level, but increased SOD activity. Cardiac superoxide and H2O2 generation were decreased in SHRs-treated group. CJID caused cardiac SODs expressions to be increased but NOXs expressions to be suppressed. In conclusion, CJID prevents H-LVH by reducing reactive oxygen species production via the NOXs-dependent pathway.