Background. The study was designed to investigate if H2S could inhibit high-salt diet-induced renal excessive oxidative stress and kidney injury in Dahl rats. Methods. Male salt-sensitive Dahl and SD rats were used. Blood pressure (BP), serum creatinine, urea, creatinine clearance rate, and 24-hour urine protein were measured. Renal ultra- and microstructures were observed. Collagen-I and -III contents the oxidants and antioxidants levels in renal tissue were detected. Keap1/Nrf2 association and Keap1 s-sulfhydration were detected. Results. After 8 weeks of high-salt diet, BP was significantly increased, renal function and structure were impaired, and collagen deposition was abundant in renal tissues with increased renal MPO activity, H2O2, MDA, GSSG, and •OH contents, reduced renal T-AOC and GSH contents, CAT, GSH-PX and SOD activity, and SOD expressions in Dahl rats. Furthermore, endogenous H2S in renal tissues was decreased in Dahl rats. H2S donor, however, decreased BP, improved renal function and structure, and inhibited collagen excessive deposition in kidney, in association with increased antioxidative activity and reduced oxidative stress in renal tissues. H2S activated Nrf2 by inducing Keap1 s-sulfhydration and subsequent Keap1/Nrf2 disassociation. Conclusions. H2S protected against high-salt diet-induced renal injury associated with enhanced antioxidant capacity and inhibited renal oxidative stress.
The study aimed to examine the protective effect of hydrogen sulfide (H2S) on high-salt-induced oxidative stress and myocardial hypertrophy in salt-sensitive (Dahl) rats. Thirty male Dahl rats and 40 SD rats were included in the study. They were randomly divided into Dahl control (Dahl + NS), Dahl high salt (Dahl + HS), Dahl + HS + NaHS, SD + NS, SD + HS, SD + HS + NaHS, and SD + HS + hydroxylamine (HA). Rats in Dahl + NS and SD + NS groups were given chow with 0.5% NaCl and 0.9% normal saline intraperitoneally daily. Myocardial structure, α-myosin heavy chain (α-MHC) and β-myosin heavy chain (β-MHC) expressions were determined. Endogenous myocardial H2S pathway and oxidative stress in myocardial tissues were tested. Myocardial H2S pathway was downregulated with myocardial hypertrophy featured by increased heart weight/body weight and cardiomyocytes cross-sectional area, decreased α-MHC and increased β-MHC expressions in Dahl rats with high-salt diet (all P < 0.01), and oxidative stress in myocardial tissues was significantly activated, demonstrated by the increased contents of hydroxyl radical, malondialdehyde and oxidized glutathione and decreased total antioxidant capacity, carbon monoxide, catalase, glutathione, glutathione peroxidase, superoxide dismutase (SOD) activities and decreased SOD1 and SOD2 protein expressions (P < 0.05, P < 0.01). However, H2S reduced myocardial hypertrophy with decreased heart weight/body weight and cardiomyocytes cross-sectional area, increased α-MHC, decreased β-MHC expressions and inhibited oxidative stress in myocardial tissues of Dahl rats with high-salt diet. However, no significant difference was found in H2S pathway, myocardial structure, α-MHC and β-MHC protein and oxidative status in myocardial tissues among SD + NS, SD + HS, and SD + HS + NaHS groups. HA, an inhibitor of cystathionine β-synthase, inhibited myocardial H2S pathway (P < 0.01), and stimulated myocardial hypertrophy and oxidative stress in SD rats with high-salt diet. Hence, H2S inhibited myocardial hypertrophy in high salt-stimulated Dahl rats in association with the enhancement of antioxidant capacity, thereby inhibiting oxidative stress in myocardial tissues.
The study was designed to investigate the role of endogenous sulfur dioxide (SO2) in collagen remodeling and its mechanisms in vascular smooth muscle cells (VSMCs). Overexpression of endogenous SO2 synthase aspartate aminotransferase (AAT) 1 or 2 increased SO2 levels and inhibited collagen I and III expressions induced by transforming growth factor (TGF)-β1 in VSMCs. In contrast, AAT1 or AAT2 knockdown induced a severe collagen deposition in TGF-β1-treated VSMCs. Furthermore, AAT1 or AAT2 overexpression suppressed procollagen I and III mRNA, upregulated matrix metalloproteinase (MMP)-13 expression, downregulated tissue inhibitors of MMP-1 level, and vice versa. Mechanistically, AAT1 or AAT2 overexpression inhibited phosphorylation of type I TGF-β receptor (TβRI) and Smad2/3 in TGF-β1-stimulated VSMCs. Whereas SB431542, an inhibitor of TGF-β1/Smad signaling pathway, attenuated excessive collagen deposition induced by AAT knockdown. Most importantly, ectopically expressing AAT or exogenous addition of 100 μM SO2 blocked AAT deficiency-aggravated collagen accumulation in TGF-β1-stimulatd VSMCs, while no inhibition was observed at 100 μM ethyl pyruvate. These findings indicated that endogenous SO2 alleviated collagen remodeling by controlling TGF-β1/TβRI/Smad2/3-mediated modulation of collagen synthesis and degradation.
Background: The number of coronavirus disease 2019 (COVID-19) cases caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has significantly increased, and the disease is rapidly spreading to all parts of the country and around the world. A retrospective study of children with SARS-CoV-2 provides a reference for the diagnosis and treatment of children during this epidemic.Methods: We retrospectively studied 12 cases of children with viral infection caused by SARS-CoV-2 admitted to 6 hospitals in Guangdong Province between January 25, 2020, and February 12, 2020, and analyzed the clinical features and outcomes of the patients.Results: A total of 12 children with SARS-CoV-2 infection from 6 hospitals were enrolled in the study; 6 were boys. The mean age was 9.8 ± 4.7 years, with a minimum age of 2 years and 10 months. The mean body weight was 37.3 ± 23.6 kg, with a minimum body weight of 13.0 kg. There were no severe cases or critical severe cases. There were 2 cases of mild pneumonia (16.7%), 7 cases of acute upper respiratory tract infection (58.3%), and 3 cases of latent infection (25.0%). In terms of symptoms, there were 7 cases of fever (58.3%), 5 cases of cough (41.7%), 3 cases of runny nose (25.0%), 2 cases of systemic fatigue and soreness (16.7%), and 4 cases of no symptoms (33.3%). Three patients (75.0%) showed decreased white blood cell (WBC) counts for their first complete blood count (CBC) after admission, and one patient (8.3%) had a low lymphocyte count. There were no obvious abnormalities in C-reactive protein (CRP, 1.53 ± 2.28 mg/l), procalcitonin (PCT, 0.21 ± 0.13 ng/ml), or coagulation function. No abnormalities were detected for creatine kinase (CK), creatine kinase-MB (CKMB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and serum creatinine (Scr). Six cases (50.0%) were positive for Mycoplasma pneumoniae antibodies. 2 cases showed pulmonary exudative lesions on chest X-ray or computed tomography (CT). All children tested positive for SARS-CoV-2 by real-time reverse-transcription–polymerase-chain-reaction (RT-PCR) assays of throat swabs. 9 patients received antiviral treatment with lopinavir/ritonavir. All patients received symptomatic supportive treatment and were quarantined, and their conditions improved. There was no respiratory failure, acute respiratory distress syndrome, shock complications, or death observed for any case. All patients recovered and were discharged, with an average length of hospital stay of 14 days.Conclusions: This study with a small sample size suggests that all SARS-CoV-2-infected children had normal or reduced WBCs; however, fever was not as common as expected, and a decrease in lymphocyte count was rare. The clinical manifestations of SARS-CoV-2 infection in children are mild, COVID⁃19 is rare, and the prognosis is good. But the presence of latent SARS-CoV-2 infection in children presents new challenges for effective clinical prevention and control.
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