17 results on '"Qi Zhu"'
Search Results
2. Tax1 banding protein 1 exacerbates heart failure in mice by activating ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis
- Author
-
Wu, Qing-qing, Yao, Qi, Hu, Tong-tong, Wan, Ying, Xie, Qing-wen, Zhao, Jin-hua, Yuan, Yuan, and Tang, Qi-zhu
- Published
- 2022
- Full Text
- View/download PDF
3. Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways
- Author
-
Li, Dan, Guo, Ying-ying, Cen, Xian-feng, Qiu, Hong-liang, Chen, Si, Zeng, Xiao-feng, Zeng, Qian, Xu, Man, and Tang, Qi-zhu
- Published
- 2022
- Full Text
- View/download PDF
4. 6-Gingerol protects against cardiac remodeling by inhibiting the p38 mitogen-activated protein kinase pathway
- Author
-
Ma, Shu-qing, Guo, Zhen, Liu, Fang-yuan, Hasan, Shahzad-Gul, Yang, Dan, Tang, Nan, An, Peng, Wang, Ming-yu, Wu, Hai-ming, Yang, Zheng, Fan, Di, and Tang, Qi-zhu
- Published
- 2021
- Full Text
- View/download PDF
5. Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target
- Author
-
Zhang, Xin, Hu, Can, Wu, Hai-ming, Ma, Zhen-guo, and Tang, Qi-zhu
- Published
- 2021
- Full Text
- View/download PDF
6. Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice
- Author
-
Zhang, Xin, Hu, Can, Zhang, Ning, Wei, Wen-ying, Li, Ling-li, Wu, Hai-ming, Ma, Zhen-guo, and Tang, Qi-zhu
- Published
- 2021
- Full Text
- View/download PDF
7. Ginsenoside Rg1 in neurological diseases: From bench to bedside
- Author
-
Shao-Jie, Yang, Jing-Ji, Wang, Ping, Cheng, Li-Xia, Chen, Jia-Min, Hu, and Guo-Qi, Zhu
- Subjects
Pharmacology ,Pharmacology (medical) ,General Medicine - Abstract
Ginseng has been used in China as a superior medicinal material for thousands of years that can nourish the five internal organs, calm the mind and benefit wisdom. Due to its anti-inflammatory, antioxidant and neuroprotective activities, one of the active components of ginseng, ginsenoside Rg1, has been extensively investigated in the remedy of brain disorders, especially dementia and depression. In this review, we summarized the research progress on the action mechanisms of Rg1 ameliorating depression-like behaviors, including inhibition of hyperfunction of hypothalamic-pituitary-adrenal (HPA) axis, regulation of synaptic plasticity and gut flora. Rg1 may alleviate Alzheimer's disease in the early phase, as well as in the middle-late phases through repairing dendrite, axon and microglia- and astrocyte-related inflammations. We also proposed that Rg1 could regulate memory state (the imbalance of working and aversive memory) caused by distinct stimuli. These laboratory studies would further the clinical trials on Rg1. From the prospective of drug development, we discussed the limitations of the present investigations and proposed our ideas to increase permeability and bioavailability of Rg1. Taken together, Rg1 has the potential to treat neuropsychiatric disorders, but a future in-depth investigation of the mechanisms is still required. In addition, drug development will benefit from the clinical trials in one specific neuropsychiatric disorder.
- Published
- 2022
8. Tax1 banding protein 1 exacerbates heart failure in mice by activating ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis
- Author
-
Qing-Qing, Wu, Qi, Yao, Tong-Tong, Hu, Ying, Wan, Qing-Wen, Xie, Jin-Hua, Zhao, Yuan, Yuan, and Qi-Zhu, Tang
- Subjects
Heart Failure ,Mice, Knockout ,Pharmacology ,Angiotensin II ,Ubiquitin-Protein Ligases ,NF-kappa B ,Membrane Proteins ,Apoptosis ,Mice, Transgenic ,Stroke Volume ,General Medicine ,Antiviral Agents ,Ventricular Function, Left ,Diabetes Mellitus, Experimental ,Rats ,Mitochondrial Proteins ,Mice ,Proto-Oncogene Proteins c-bcl-2 ,Animals ,Myocytes, Cardiac ,Pharmacology (medical) - Abstract
Tax1 banding protein 1 (Tax1bp1) was originally identified as an NF-κB regulatory protein that participated in inflammatory, antiviral and innate immune processes. Tax1bp1 also functions as an autophagy receptor that plays a role in autophagy. Our previous study shows that Tax1bp1 protects against cardiomyopathy in STZ-induced diabetic mice. In this study we investigated the role of Tax1bp1 in heart failure. Pressure overload-induced heart failure model was established in mice by aortic banding (AB) surgery, and angiotensin II (Ang II)-induced heart failure model was established by infusion of Ang II through osmotic minipump for 4 weeks. We showed that the expression levels of Tax1bp1 in the heart were markedly increased 2 and 4 weeks after AB surgery. Knockdown of Tax1bp1 in mouse hearts significantly ameliorated both AB- and Ang II infusion-induced heart failure parameters. On the contrary, AB-induced heart failure was aggravated in cardiac-specific Tax1bp1 transgenic mice. Similar results were observed in neonatal rat cardiomyocytes (NRCMs) under Ang II insult. We demonstrated that the pro-heart failure effect of Tax1bp1 resulted from its interaction with the E3 ligase ITCH to promote the transcription factor P73 ubiquitination and degradation, causing enhanced BCL2 interacting protein 3 (BNIP3)-mediated cardiomyocyte apoptosis. Knockdown ITCH or BNIP3 in NRCMs significantly reduced Ang II-induced apoptosis in vitro. Similarly, BNIP3 knockdown attenuated heart failure in cardiac-specific Tax1bp1 transgenic mice. In the left ventricles of heart failure patients, Tax1bp1 expression level was significantly increased; Tax1bp1 gene expression was negatively correlated with left ventricular ejection fraction in heart failure patients. Collectively, the Tax1bp1 increase in heart failure enhances ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis and induced cardiac injury. Tax1bp1 may serve as a potent therapeutic target for the treatment of heart failure.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Knockout of Tax1bp1 in mouse hearts ameliorated heart failure induced by pressure overload.• Tax1bp1 interacts with the E3 ligase Itch to promote P73 ubiquitination and degradation, causing enhanced BNIP3-mediated apoptosis.• Tax1bp1 may become a target of new therapeutic methods for treating heart failure.
- Published
- 2022
9. Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways
- Author
-
Dan, Li, Ying-Ying, Guo, Xian-Feng, Cen, Hong-Liang, Qiu, Si, Chen, Xiao-Feng, Zeng, Qian, Zeng, Man, Xu, and Qi-Zhu, Tang
- Subjects
Pharmacology ,NF-kappa B ,Cardiomegaly ,General Medicine ,Rats ,Mice, Inbred C57BL ,Toll-Like Receptor 4 ,Mice ,Phosphatidylinositol 3-Kinases ,Animals ,Myocytes, Cardiac ,Pharmacology (medical) ,Pentacyclic Triterpenes ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
Inflammation and apoptosis are main pathological processes that lead to the development of cardiac hypertrophy. Lupeol, a natural triterpenoid, has shown anti-inflammatory and anti-apoptotic activities as well as potential protective effects on cardiovascular diseases. In this study we investigated whether lupeol attenuated cardiac hypertrophy and fibrosis induced by pressure overload in vivo and in vitro, and explored the underlying mechanisms. Cardiac hypertrophy was induced in mice by transverse aortic constriction (TAC) surgery, and in neonatal rat cardiomyocytes (NRCMs) by stimulation with phenylephrine (PE) in vitro. We showed that administration of lupeol (50 mg ·kg
- Published
- 2021
10. Anti-PD-L1 mediating tumor-targeted codelivery of liposomal irinotecan/JQ1 for chemo-immunotherapy
- Author
-
Yonghui Wang, Yongzhuo Huang, Binfan Chen, Yang He, Bin Tu, Meng Zhang, Si-qi Zhu, Zhi-di He, and Hairui Wang
- Subjects
0301 basic medicine ,Combination therapy ,medicine.medical_treatment ,Programmed Cell Death 1 Receptor ,chemical and pharmacologic phenomena ,Irinotecan ,T-Lymphocytes, Regulatory ,Article ,B7-H1 Antigen ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Cell Line, Tumor ,Neoplasms ,Antineoplastic Combined Chemotherapy Protocols ,Tumor Microenvironment ,medicine ,Animals ,Pharmacology (medical) ,Immune Checkpoint Inhibitors ,Pharmacology ,Mice, Inbred BALB C ,business.industry ,FOXP3 ,Azepines ,General Medicine ,Immunotherapy ,Triazoles ,Immune checkpoint ,030104 developmental biology ,030220 oncology & carcinogenesis ,Cancer research ,Immunogenic cell death ,Liposomal Irinotecan ,Female ,business ,medicine.drug - Abstract
Immune checkpoint blockade therapy has become a first-line treatment in various cancers. But there are only a small percent of colorectal patients responding to PD-1/PD-L1 blockage immunotherapy. How to increase their treatment efficacy is an urgent and clinically unmet need. It is acknowledged that immunogenic cell death (ICD) induced by some specific chemotherapy can enhance antitumor immunity. Chemo-based combination therapy can yield improved outcomes by activating the immune system to eliminate the tumor, compared with monotherapy. Here, we develop a PD-L1-targeting immune liposome (P-Lipo) for co-delivering irinotecan (IRI) and JQ1, and this system can successfully elicit antitumor immunity in colorectal cancer through inducing ICD by IRI and interfering in the immunosuppressive PD-1/PD-L1 pathway by JQ1. P-Lipo increases intratumoral drug accumulation and promotes DC maturation, and thereby facilitates adaptive immune responses against tumor growth. The remodeling tumor immune microenvironment was reflected by the increased amount of CD8(+) T cells and the release of IFN-γ, and the reduced CD4(+)Foxp3(+) regulatory T cells (Tregs). Collectively, the P-Lipo codelivery system provides a chemo-immunotherapy strategy that can effectively remodel the tumor immune microenvironment and activate the host immune system and arrest tumor growth.
- Published
- 2020
11. Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways
- Author
-
Li, Dan, primary, Guo, Ying-ying, additional, Cen, Xian-feng, additional, Qiu, Hong-liang, additional, Chen, Si, additional, Zeng, Xiao-feng, additional, Zeng, Qian, additional, Xu, Man, additional, and Tang, Qi-zhu, additional
- Published
- 2021
- Full Text
- View/download PDF
12. β-Arrestin 2 mediates arginine vasopressin-induced IL-6 induction via the ERK1/2-NF-κB signal pathway in murine hearts
- Author
-
Hong Cao, Na Yao, Lingling Zhao, Xiaofang Zhu, Qi Zhu, Eran Ni, Shuzhen Sun, and Weizhong Zhu
- Subjects
0301 basic medicine ,Pharmacology ,Vasopressin ,Gene knockdown ,medicine.medical_specialty ,Arginine ,medicine.drug_class ,medicine.medical_treatment ,NF-κB ,General Medicine ,Receptor antagonist ,03 medical and health sciences ,chemistry.chemical_compound ,030104 developmental biology ,0302 clinical medicine ,Endocrinology ,Cytokine ,chemistry ,030220 oncology & carcinogenesis ,Internal medicine ,medicine ,Phosphorylation ,Pharmacology (medical) ,Signal transduction ,hormones, hormone substitutes, and hormone antagonists - Abstract
Evidence to date suggests that β-arrestins act beyond their role as adapter proteins. Arginine vasopressin (AVP) may be a factor in inflammation and fibrosis in the pathogenesis of heart failure. In the present study we investigated the effect of AVP on inflammatory cytokine IL-6 production in murine hearts and the impact of β-arrestin 2-dependent signaling on AVP-induced IL-6 production. We found that administration of AVP (0.5 U/kg, iv) markedly increased the levels of IL-6 mRNA in rat hearts with the maximum level occurred at 6 h. In β-arrestin 2 KO mouse hearts, deletion of β-arrestin 2 decreased AVP-induced IL-6 mRNA expression. We then performed in vitro experiments in adult rat cardiac fibroblasts (ARCFs). We found that AVP (10−9–10−6 M) dose-dependently increased the expression of IL-6 mRNA and protein, activation of NF-κB signaling and ERK1/2 phosphorylation, whereas knockdown of β-arrestin 2 blocked AVP-induced IL-6 increase, NF-κB activation and ERK1/2 phosphorylation. Pharmacological blockade of ERK1/2 using PD98059 diminished AVP-induced NF-κB activation and IL-6 production. The selective V1A receptor antagonist SR49059 effectively blocked AVP-induced NF-κB phosphorylation and activation as well as IL-6 expression in ARCFs. In AVP-treated mice, pre-injection of SR49059 (2 mg/kg, iv) abolished AVP-induced NF-κB activation and IL-6 production in hearts. The above results suggest that AVP induces IL-6 induction in murine hearts via the V1A receptor-mediated β-arrestin2/ERK1/2/NF-κB pathway, thus reveal a novel mechanism of myocardial inflammation in heart failure involving the V1A/β-arrestin 2/ERK1/2/NF-κB signaling pathway.
- Published
- 2019
13. Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice
- Author
-
Hai-Ming Wu, Ling-Li Li, Wen-Ying Wei, Qi-Zhu Tang, Can Hu, Zhen-Guo Ma, Ning Zhang, and Xin Zhang
- Subjects
Male ,Ribosomal Proteins ,Cardiotonic Agents ,Cardiac fibrosis ,MAP Kinase Signaling System ,p38 mitogen-activated protein kinases ,Pharmacology ,medicine.disease_cause ,p38 Mitogen-Activated Protein Kinases ,Article ,chemistry.chemical_compound ,Alkaloids ,Downregulation and upregulation ,Matrine ,In vivo ,Cell Movement ,Isoprenaline ,medicine ,Animals ,Pharmacology (medical) ,Matrines ,Cell Proliferation ,business.industry ,Isoproterenol ,Heart ,General Medicine ,Fibroblasts ,medicine.disease ,Fibrosis ,Up-Regulation ,Mice, Inbred C57BL ,chemistry ,Heart failure ,Cell Transdifferentiation ,business ,Cardiomyopathies ,Oxidative stress ,Quinolizines ,medicine.drug - Abstract
Pathological cardiac fibrosis is a common feature in multiple cardiovascular diseases that contributes to the occurrence of heart failure and life-threatening arrhythmias. Our previous study demonstrated that matrine could attenuate doxorubicin-induced oxidative stress and cardiomyocyte apoptosis. In this study, we investigated the effect of matrine on cardiac fibrosis. Mice received aortic banding (AB) operation or continuous injection of isoprenaline (ISO) to generate pathological cardiac fibrosis and then were exposed to matrine lavage (200 mg·kg −1 ·d −1 ) or an equal volume of vehicle as the control. We found that matrine lavage significantly attenuated AB or ISO-induced fibrotic remodeling and cardiac dysfunction. We also showed that matrine (200 μmol/L) significantly inhibited the proliferation, migration, collagen production, and phenotypic transdifferentiation of cardiac fibroblasts. Mechanistically, matrine suppressed p38 activation in vivo and in vitro, and overexpression of constitutively active p38 completely abolished the protective effects of matrine. We also demonstrated that ribosomal protein S5 (RPS5) upregulation was responsible for matrine-mediated inhibition on p38 and fibrogenesis. More importantly, matrine was capable of ameliorating preexisting cardiac fibrosis in mice. In conclusion, matrine treatment attenuates cardiac fibrosis by regulating RPS5/p38 signaling in mice, and it might be a promising therapeutic agent for treating pathological cardiac fibrosis.
- Published
- 2020
14. Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target
- Author
-
Zhang, Xin, primary, Hu, Can, additional, Wu, Hai-ming, additional, Ma, Zhen-guo, additional, and Tang, Qi-zhu, additional
- Published
- 2020
- Full Text
- View/download PDF
15. Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice
- Author
-
Zhang, Xin, primary, Hu, Can, additional, Zhang, Ning, additional, Wei, Wen-ying, additional, Li, Ling-li, additional, Wu, Hai-ming, additional, Ma, Zhen-guo, additional, and Tang, Qi-zhu, additional
- Published
- 2020
- Full Text
- View/download PDF
16. β-Arrestin 2 mediates arginine vasopressin-induced IL-6 induction via the ERK
- Author
-
Shu-Zhen, Sun, Hong, Cao, Na, Yao, Ling-Ling, Zhao, Xiao-Fang, Zhu, Er-An, Ni, Qi, Zhu, and Wei-Zhong, Zhu
- Subjects
Heart Failure ,Male ,Mice, Knockout ,Mitogen-Activated Protein Kinase 1 ,Receptors, Vasopressin ,myocardial inflammation ,IL-6 ,Mitogen-Activated Protein Kinase 3 ,Dose-Response Relationship, Drug ,ERK1/2 ,Interleukin-6 ,β-Arrestin 2 ,NF-kappa B ,Heart ,Fibroblasts ,adult rat cardiac fibroblasts ,beta-Arrestin 2 ,Article ,Rats ,Arginine Vasopressin ,Rats, Sprague-Dawley ,Mice ,Gene Knockdown Techniques ,Animals ,hormones, hormone substitutes, and hormone antagonists - Abstract
Evidence to date suggests that β-arrestins act beyond their role as adapter proteins. Arginine vasopressin (AVP) may be a factor in inflammation and fibrosis in the pathogenesis of heart failure. In the present study we investigated the effect of AVP on inflammatory cytokine IL-6 production in murine hearts and the impact of β-arrestin 2-dependent signaling on AVP-induced IL-6 production. We found that administration of AVP (0.5 U/kg, iv) markedly increased the levels of IL-6 mRNA in rat hearts with the maximum level occurred at 6 h. In β-arrestin 2 KO mouse hearts, deletion of β-arrestin 2 decreased AVP-induced IL-6 mRNA expression. We then performed in vitro experiments in adult rat cardiac fibroblasts (ARCFs). We found that AVP (10−9–10−6 M) dose-dependently increased the expression of IL-6 mRNA and protein, activation of NF-κB signaling and ERK1/2 phosphorylation, whereas knockdown of β-arrestin 2 blocked AVP-induced IL-6 increase, NF-κB activation and ERK1/2 phosphorylation. Pharmacological blockade of ERK1/2 using PD98059 diminished AVP-induced NF-κB activation and IL-6 production. The selective V1A receptor antagonist SR49059 effectively blocked AVP-induced NF-κB phosphorylation and activation as well as IL-6 expression in ARCFs. In AVP-treated mice, pre-injection of SR49059 (2 mg/kg, iv) abolished AVP-induced NF-κB activation and IL-6 production in hearts. The above results suggest that AVP induces IL-6 induction in murine hearts via the V1A receptor-mediated β-arrestin2/ERK1/2/NF-κB pathway, thus reveal a novel mechanism of myocardial inflammation in heart failure involving the V1A/β-arrestin 2/ERK1/2/NF-κB signaling pathway.
- Published
- 2019
17. Enhanced NMDA receptor NR1 phosphorylation and neuronal activity in the arcuate nucleus of hypothalamus following peripheral inflammation
- Author
-
Xinghong Jiang, Xian-Min Yu, Gen-cheng Wu, Shan Gong, Jian-ming Peng, Qi Zhu, Long-sheng Xu, Shi-yu Guo, and Jin Tao
- Subjects
Male ,medicine.medical_specialty ,N-Methylaspartate ,Blotting, Western ,Glutamic Acid ,Receptors, N-Methyl-D-Aspartate ,chemistry.chemical_compound ,Arcuate nucleus ,Internal medicine ,medicine ,Premovement neuronal activity ,Animals ,Pharmacology (medical) ,Phosphorylation ,Rats, Wistar ,Receptor ,Pharmacology ,6-Cyano-7-nitroquinoxaline-2,3-dione ,Inflammation ,Chemistry ,musculoskeletal, neural, and ocular physiology ,Arcuate Nucleus of Hypothalamus ,General Medicine ,Glutamic acid ,Rats ,Endocrinology ,nervous system ,Receptors, Glutamate ,Hypothalamus ,CNQX ,NMDA receptor ,Original Article ,sense organs ,Dizocilpine Maleate - Abstract
Aim:To investigate the role of glutamate and N-methyl-D-aspartate (NMDA) receptors in central sensitization following peripheral inflammation in the arcuate nucleus (ARC) of the mediobasal hypothalamus.Mediobasal hypothalamic slices were prepared from rats undergoing peripheral inflammation, which was induced by a unilateral injection of complete Freund's adjuvant (CFA) into hind paw. Neuronal activation levels in the ARC were monitored by recording extracellular unit discharges. The NMDA receptor NR1 subunit (NR1) was measured using Western blot analysis.Enhanced NR1 phosphorylation was observed in the ARC of CFA-inflamed rats. Compared with the control rats, the firing rate of spontaneous discharges in ARC neurons of inflamed rats was significantly higher, and it was significantly reduced both by an NMDA receptor antagonist (MK-801, 300 μmol/L) and by a non-NMDA receptor antagonist (CNQX, 30 μmol/L). Application of exogenous glutamate (200 μmol/L) or NMDA (25 μmol/L) resulted in increased neuronal discharges for ARC neurons, which was enhanced to a greater extent in inflamed rats than in control rats.Glutamate receptor activation in the hypothalamic ARC plays a crucial role in central sensitization associated with peripheral inflammation.
- Published
- 2011
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.