5 results on '"Lerong Chen"'
Search Results
2. 3‐ O ‐trans‐caffeoyloleanolic acid improves acute lung injury via anti‐inflammation and antioxidative stress‐involved PI3K/AKT pathway
- Author
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Jianhua Huang, Xueping Nong, Yanling Chen, Aimei Zhang, and Lerong Chen
- Subjects
Lipopolysaccharides ,Male ,Phosphopeptides ,Lipopolysaccharide ,Acute Lung Injury ,Anti-Inflammatory Agents ,Nitric Oxide Synthase Type II ,Inflammation ,Pharmacology ,Lung injury ,medicine.disease_cause ,01 natural sciences ,Biochemistry ,Phosphatidylinositol 3-Kinases ,chemistry.chemical_compound ,In vivo ,Drug Discovery ,medicine ,Animals ,Humans ,Oleanolic Acid ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Mice, Inbred BALB C ,010405 organic chemistry ,Chemistry ,Macrophages ,Organic Chemistry ,0104 chemical sciences ,Toll-Like Receptor 4 ,Oxidative Stress ,010404 medicinal & biomolecular chemistry ,Gene Expression Regulation ,TLR4 ,Molecular Medicine ,medicine.symptom ,Proto-Oncogene Proteins c-akt ,Oxidative stress ,Signal Transduction - Abstract
3-O-trans-caffeoyloleanolic acid (COA) is a pentacyclic triterpenoid compound, with significant anti-inflammatory effects. In this study, we report the protective effects of COA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explored its mechanism of action. LPS was used to construct in vivo mouse ALI models to observe the effects of COA pretreatment on lung pathology, inflammation, and oxidative stress. In vitro, mouse alveolar macrophages MH-S cells were cultured and stimulated with LPS to investigate the effects of COA pretreatment on inflammation and oxidative stress. Western blotting was used to investigate the expression of iNOS, TLR4, p-p65, p-AKT, and p-PI3K from in vivo and in vitro samples. The results showed that COA significantly improved lung injury, inhibited neutrophil infiltration, prevented macrophage infiltration, inhibited the release of inflammatory factors, reduced oxidative stress, and down-regulated the expression of iNOS, TLR4, p-p65, p-AKT, and p-PI3K in ALI mice caused by LPS. In vitro, COA inhibited the release of inflammatory factors, reduced oxidative stress, and down-regulated the expression of iNOS, TLR4, p-p65, p-AKT, and p-PI3K in MH-S cells stimulated with LPS. Of interest, the protective effects of COA were significantly attenuated in MH-S cells pretreated with the PI3K phosphopeptide activator 740Y-P with no effect on TLR4 expression observed. Taken together, these findings confirm the protective effects of COA on ALI. We further demonstrate that the anti-inflammation and antioxidant effects of COA are mediated through its effects on PI3K/AKT and potentially TLR4.
- Published
- 2021
3. Curcumol Suppresses CCF-Mediated Hepatocyte Senescence Through Blocking LC3B-Lamin B1 Interaction in Alcoholic Fatty Liver Disease
- Author
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Xiaoyu Qi, Shuguo Zheng, Mingyue Ma, Naqi Lian, Hongting Wang, Lerong Chen, Anping Song, Chunfeng Lu, Shizhong Zheng, and Huanhuan Jin
- Subjects
Pharmacology ,Pharmacology (medical) - Abstract
Recent studies indicated that hepatocyte senescence plays an important role in the development of alcoholic fatty liver disease (AFLD), suggesting that inhibition of hepatocyte senescence might be a potential strategy for AFLD treatment. The present study investigated the effect of curcumol, a component from the root of Rhizoma Curcumae, on hepatocyte senescence in AFLD and the underlying mechanisms implicated. The results showed that curcumol was able to reduce lipid deposition and injury in livers of ethanol liquid diet-fed mice and in ethanol-treated LO2 cells. Both in vivo and in vitro studies indicated that supplementation with curcumol effectively alleviated ethanol-induced cellular senescence as manifested by a decrease in senescence-associated β-galactosidase (SA-β-gal) activity, a downregulated expression of senescence-related markers p16 and p21, and dysfunction of the telomere and telomerase system. Consistently, treatment with curcumol led to a marked suppression of ethanol-induced formation of cytoplasmic chromatin fragments (CCF) and subsequent activation of cGAS-STING, resulting in a significant reduction in senescence-associated secretory phenotype (SASP)-related inflammatory factors’ secretion. Further studies indicated that curcumol’s inhibition of CCF formation might be derived from blocking the interaction of LC3B with lamin B1 and maintaining nuclear membrane integrity. Taken together, these results indicated that curcumol was capable of ameliorating AFLD through inhibition of hepatocyte senescence, which might be attributed to its blocking of LC3B and lamin B1 interaction and subsequent inactivation of the CCF-cGAS-STING pathway. These findings suggest a promising use of curcumol in the treatment of AFLD.
- Published
- 2022
4. Effects of deglycosylation and the Maillard reaction on conformation and allergenicity of the egg ovomucoid
- Author
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Junjie Ma, Lerong Chen, Jinru Zhou, Yanbo Wang, Linglin Fu, and Hong Zhang
- Subjects
Male ,Glycosylation ,030309 nutrition & dietetics ,Food Handling ,Eggs ,Molecular Conformation ,Oligosaccharides ,Ovomucin ,03 medical and health sciences ,symbols.namesake ,chemistry.chemical_compound ,0404 agricultural biotechnology ,Egg White ,Glycation ,Animals ,Humans ,Egg Hypersensitivity ,0303 health sciences ,Chemistry ,Galactooligosaccharide ,Fructooligosaccharide ,Hypoallergenic ,04 agricultural and veterinary sciences ,Allergens ,040401 food science ,Maillard Reaction ,Maillard reaction ,Biochemistry ,symbols ,Chickens ,Food Science ,Egg white - Abstract
Ovomucoid (OVM), known as the major allergen in egg white, has gained increasing concerns in industrialized countries. Here, we found the deglycosylation and Maillard reaction with galactooligosaccharide (GOS) and fructooligosaccharide (FOS) can induce conformational transformation of OVM from other structures (β-turn, strang, and random coils) to α-helix. We also introduced an approach to reduce the allergenicity of Gallus domesticus OVM by Maillard reaction with GOS and FOS. However, the OVM glycated by mannosan (MOS) and deglycosylated OVM exhibited higher allergenicity than native OVM. Therefore, GOS and FOS, especially GOS, could be applied in the reduction of the potential allergenicity of OVM through glycation. Furthermore, these findings may provide new insights into the development of hypoallergenic egg products. PRACTICAL APPLICATION: In this study, the allergenicity and conformation of OVM treated with deglycosylation and glycation (GOS, FOS, and MOS) were investigated. The results would provide a better understanding of the effects of deglycosylation and Maillard reaction with different reducing sugars on the molecular characteristics of OVM and further provide new insights into the development of hypoallergenic egg products.
- Published
- 2021
5. Effects of 1,25-Dihydroxyvitamin D3 on the Prevention of Chronic Obstructive Pulmonary Disease (COPD) in Rats Exposed to Air Pollutant Particles Less than 2.5 Micrometers in Diameter (PM2.5)
- Author
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Xiaolan Yuan, Lerong Chen, Luru Zou, Xinchun Hu, and Jianping Peng
- Subjects
Male ,0301 basic medicine ,medicine.medical_specialty ,Calcitriol ,Apoptosis ,Lung injury ,Pulmonary Disease, Chronic Obstructive ,03 medical and health sciences ,0302 clinical medicine ,Air Pollution ,Internal medicine ,medicine ,Animals ,Rats, Wistar ,Lung ,COPD ,TUNEL assay ,business.industry ,Kinase ,Animal Study ,Lung Injury ,General Medicine ,medicine.disease ,Rats ,respiratory tract diseases ,Disease Models, Animal ,Treatment Outcome ,030104 developmental biology ,medicine.anatomical_structure ,Endocrinology ,Terminal deoxynucleotidyl transferase ,030220 oncology & carcinogenesis ,Particulate Matter ,business ,Bronchoalveolar Lavage Fluid ,medicine.drug - Abstract
BACKGROUND This study aimed to investigate the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on airway changes in chronic obstructive pulmonary disease (COPD) rats exposed to air pollutant particles less than 2.5 micrometers in diameter (PM2.5), and to evaluate the mechanisms. MATERIAL AND METHODS Three groups were included in this study: a normal group, a COPD model group, and a COPD with 1,25(OH)2D3 treatment group. In each group, the rats were divided into four subgroups: control and different doses of PM2.5 (1.6, 8 and 40 mg/kg body weight). Apoptosis in lung tissue was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). The expression of c-Jun N-terminal kinase 1 (JNK1) and mucin 5AC (MUC5AC) were detected by real-time polymerase chain reaction (RT-PCR), Western blotting and immunofluorescence staining. RESULTS Compared with corresponding subgroups in normal group, the apoptotic rates in COPD group were significantly increased. By contrast, 1,25(OH)2D3 treatment group significantly reduced COPD-induced apoptosis in lung tissue. Upon the dose increase of PM2.5, the apoptotic rate was also elevated in each group. Compared with the corresponding control in each group, PM2.5 increased apoptosis in a dose-dependent manner. Importantly, 1,25(OH)2D3 also prevented apoptosis in COPD rats exposed to PM2.5. Mechanically, the expression of MUC5AC and JNK1 in COPD group was significantly upregulated, compared with corresponding subgroups in the normal group. Treatment with 1,25(OH)2D3 reduced expression of MUC5AC and JNK1 in COPD rats. It was found that the expression of MUC5AC and JNK1 was elevated with the dose increase of PM2.5 in each group. Consistently, 1,25(OH)2D3 also reduced the expression of MUC5AC and JNK1 in COPD rats exposed to PM2.5. CONCLUSIONS 1,25(OH)2D3 prevented lung injury in COPD rats with or without PM2.5 exposure. Our results suggest that 1,25(OH)2D3 is useful to mitigate the injury caused by COPD.
- Published
- 2018
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