6 results on '"Caixia Dou"'
Search Results
2. Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition
- Author
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Jianyu Liu, Minghai Tang, Tao Li, Zhengying Su, Zejiang Zhu, Caixia Dou, Yan Liu, Heying Pei, Jianhong Yang, Haoyu Ye, and Lijuan Chen
- Subjects
heart failure ,myocardial infarction ,honokiol ,reactive oxygen species ,UCP3 ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Post-myocardial infarction heart failure (post-MI HF) is one of the leading global causes of death, and current prevention and treatment methods still cannot avoid the increasing incidence. Honokiol (HK) has previously been reported to improve myocardial ischemia/reperfusion injury and reverse myocardial hypertrophy by activating Sirt1 and Sirt3. We suspect that HK may also have a therapeutic effect on post-MI HF. In this study, we aimed to investigate the efficacy and mechanism of HK in the treatment of post-MI HF. We found that HK inhibited myocardial reactive oxygen species (ROS) production, reduced myocardial fibrosis, and improved cardiac function in mice after MI. HK also reduced the abnormality of mitochondrial membrane potential (MMP) and apoptosis of cardiomyocytes caused by peroxide in neonatal cardiomyocytes. RNAseq results revealed that HK restored the transcriptome changes to a certain extent and significantly enhanced the expression of mitochondrial inner membrane uncoupling protein isoform 3 (Ucp3), a protein that inhibits the production of mitochondrial ROS, protects cardiomyocytes, and relieves heart failure after myocardial infarction (MI). In cardiomyocytes with impaired Ucp3 expression, HK cannot protect against the damage caused by peroxide. More importantly, in Ucp3 knockout mice, HK did not change the increase in the ROS level and cardiac function damage after MI. Taken together, our results suggest that HK can increase the expression of the cardioprotective protein Ucp3 and maintain MMP, thereby inhibiting the production of ROS after MI and ameliorating heart failure.
- Published
- 2022
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3. β-Elemene-loaded polymeric micelles intensify anti-carcinoma efficacy and alleviate side effects
- Author
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Zejiang Zhu, Caixia Dou, Lijuan Chen, Qiaoqiao Hu, Peng Bai, Rongsheng Tong, Zhengying Su, Lulu Cai, Bai Lan, Junfeng Yan, Wuyu Zhang, and Minghai Tang
- Subjects
Tube formation ,Drug ,Chemistry ,media_common.quotation_subject ,02 engineering and technology ,General Chemistry ,Pharmacology ,010402 general chemistry ,021001 nanoscience & nanotechnology ,01 natural sciences ,Micelle ,0104 chemical sciences ,Bioavailability ,chemistry.chemical_compound ,Pharmacokinetics ,Drug delivery ,Toxicity ,0210 nano-technology ,Elemene ,media_common - Abstract
β-Elemene is a volatile oil used for the treatment of cancer, but poor solubility, low bioavailability, and various adverse reactions limit its application. For ameliorating risks of the venous toxicity of β-elemene, intravenously injectable micelle of β-elemene was prepared using the thin-film hydration method. The results pointed out the micelles were uniformly spherical with about 20.96 ± 0.1966 nm in average diameter and exhibited high entrapment efficiency (99.02% ± 0.88%). As revealed by drug release studies in vitro, β-elemene micelles had sustained drug release. Compared with free β-elemene, the micelles increased the drug cellular uptake and enhanced the anti-tumor effect in vitro through retarding cell cycle and inducing apoptosis. Meanwhile, the elevated serum stability of β-elemene micelles implied less drug leakage and reduced toxicity. The wound healing and tube formation assay in vitro demonstrated the anti-metastasis and anti-angiogenesis effects of β-elemene micelles. Moreover, the pharmacokinetics study showed the AUC and T1/2 of β-elemene in micelle group were 1.79 and 1.62 times of that in free β-elemene group, suggesting the circulation time of β-elemene in the blood had been prolonged. In addition, β-elemene micelles showed a favorable antitumor response compared with the β-elemene solution on C26 colon cancer-bearing mice model. Local irritation study investigated in rabbits indicated that the β-elemene micelles strikingly mitigated the irritation to the injection sites compared with free β-elemene. These results proved that the micelle could be a good candidate as an auspicious drug delivery system of β-elemene for the prospective clinical treatment of carcinoma.
- Published
- 2020
4. Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition
- Author
-
Jianyu Liu, Minghai Tang, Tao Li, Zhengying Su, Zejiang Zhu, Caixia Dou, Yan Liu, Heying Pei, Jianhong Yang, Haoyu Ye, and Lijuan Chen
- Subjects
Pharmacology ,Pharmacology (medical) - Abstract
Post-myocardial infarction heart failure (post-MI HF) is one of the leading global causes of death, and current prevention and treatment methods still cannot avoid the increasing incidence. Honokiol (HK) has previously been reported to improve myocardial ischemia/reperfusion injury and reverse myocardial hypertrophy by activating Sirt1 and Sirt3. We suspect that HK may also have a therapeutic effect on post-MI HF. In this study, we aimed to investigate the efficacy and mechanism of HK in the treatment of post-MI HF. We found that HK inhibited myocardial reactive oxygen species (ROS) production, reduced myocardial fibrosis, and improved cardiac function in mice after MI. HK also reduced the abnormality of mitochondrial membrane potential (MMP) and apoptosis of cardiomyocytes caused by peroxide in neonatal cardiomyocytes. RNAseq results revealed that HK restored the transcriptome changes to a certain extent and significantly enhanced the expression of mitochondrial inner membrane uncoupling protein isoform 3 (Ucp3), a protein that inhibits the production of mitochondrial ROS, protects cardiomyocytes, and relieves heart failure after myocardial infarction (MI). In cardiomyocytes with impaired Ucp3 expression, HK cannot protect against the damage caused by peroxide. More importantly, in Ucp3 knockout mice, HK did not change the increase in the ROS level and cardiac function damage after MI. Taken together, our results suggest that HK can increase the expression of the cardioprotective protein Ucp3 and maintain MMP, thereby inhibiting the production of ROS after MI and ameliorating heart failure.
- Published
- 2021
5. Clostridium butyricum Protects IPEC-J2 Cells from ETEC K88-Induced Oxidative Damage by Activating the Nrf2/ARE Signaling Pathway
- Author
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Zhiyuan Shang, Caixia Dou, Jiayun Qiao, Yimeng Wang, and Haihua Li
- Subjects
0301 basic medicine ,Aging ,GPX1 ,GPX2 ,Article Subject ,SOD2 ,medicine.disease_cause ,Biochemistry ,digestive system ,Superoxide dismutase ,03 medical and health sciences ,0302 clinical medicine ,Enterotoxigenic Escherichia coli ,medicine ,Viability assay ,Clostridium butyricum ,biology ,QH573-671 ,Chemistry ,Cell Biology ,General Medicine ,biology.organism_classification ,Molecular biology ,030104 developmental biology ,biology.protein ,Cytology ,030217 neurology & neurosurgery ,Oxidative stress ,Research Article - Abstract
Clostridium butyricum (CB) is a naturally occurring probiotic compound that can alleviate the oxidative damage induced by enterotoxigenic Escherichia coli K88 (ETEC K88) in porcine intestinal epithelial (IPEC-J2) cells. In this study, we investigate the molecular mechanism underlying this effect. Based on cell viability, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) assessments, the optimal concentration of ETEC K88 was determined to be 1 × 10 3 cfu/mL. Viable bacteria counts in cells pretreated with CB and then infected with ETEC K88 show that CB can adhere to IPEC-J2 cells and that optimal adhesion is achieved at the multiple infection index (MOI) of 50 at 3 h of pretreatment. The results of qPCR indicate that although ETEC significantly decreases the expression levels of antioxidant enzymes regulated by NF-E2-related factor 2 (Nrf2) compared to the control group, CB reverses this effect. To confirm that Nrf2 is directly involved in the mechanism by which CB alleviates oxidative stress, siRNA was used to silence the expression of Nrf2 gene in IPEC-J2 cells. Compared to the NC+ETEC and siRNA+ETEC groups, the expressions of SOD1, SOD2, GPX1, and GPX2 in the NC+CB+ETEC and siRNA+CB+ETEC groups are significantly increased at 12 h and 24 h. This shows that CB can reduce ETEC K88-induced oxidative damage in IPEC-J2 cells by activating the expression of antioxidant enzymes implicated in the Kelch-like ECH-associated protein-1- (Keap1-) Nrf2/antioxidant response element (ARE) signaling pathway.
- Published
- 2021
6. Identification of Pyrrolo[2,3-d]pyrimidine-Based Derivatives as Potent and Orally Effective Fms-like Tyrosine Receptor Kinase 3 (FLT3) Inhibitors for Treating Acute Myelogenous Leukemia
- Author
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Wanhua Zhang, Tao Yang, Yuquan Wei, Linyu Yang, Aihua Peng, Shengyong Yang, Jun He, Minghai Tang, Haoyu Ye, Lei Lei, Ting Niu, Caixia Dou, Muzhou Li, Lijuan Chen, Mingli Xiang, Yong Chen, Jiang Liu, and Xue Yuan
- Subjects
Administration, Oral ,Apoptosis ,Pharmacology ,01 natural sciences ,Mice ,Structure-Activity Relationship ,03 medical and health sciences ,Myelogenous ,chemistry.chemical_compound ,Cell Line, Tumor ,Drug Discovery ,medicine ,Animals ,Humans ,Cytotoxic T cell ,Pyrroles ,Benzothiazoles ,Protein Kinase Inhibitors ,030304 developmental biology ,Quizartinib ,0303 health sciences ,Binding Sites ,Kinase ,Phenylurea Compounds ,medicine.disease ,G1 Phase Cell Cycle Checkpoints ,Xenograft Model Antitumor Assays ,0104 chemical sciences ,Molecular Docking Simulation ,Leukemia, Myeloid, Acute ,Proto-Oncogene Proteins c-kit ,010404 medicinal & biomolecular chemistry ,Leukemia ,Pyrimidines ,fms-Like Tyrosine Kinase 3 ,chemistry ,Drug Resistance, Neoplasm ,Cell culture ,Drug Design ,Cancer cell ,Molecular Medicine ,Half-Life - Abstract
A series of pyrrolo[2,3- d]pyrimidine derivatives were prepared and optimized for cytotoxic activities against FLT3-ITD mutant cancer cells. Among them, compound 9u possessed nanomolar FLT3 inhibitory activities and subnanomolar inhibitory activities against MV4-11 and Molm-13 cells. It also showed excellent inhibitory activities in FLT3-ITD-D835V and FLT3-ITD-F691L cells which were resistant to quizartinib. Furthermore, 9u exhibited over 40-fold selectivity toward FLT3 relative to c-Kit kinase, which might reduce myelosuppression toxicity. Cellular assays demonstrated that 9u inhibited phosphorylated FLT3 and downstream signaling factors and also induced cell cycle arrest in the G0/G1 stage and apoptosis in MV4-11 and Molm-13 cells. Oral administration of 9u at 10 mg/kg could achieve rapid tumor extinction in the MV4-11 xenograft model and significantly inhibit the tumor growth in the MOLM-13 xenograft model with a tumor growth inhibitory rate of 96% without obvious toxicity. Additionally, 9u demonstrated high bioavailability ( F = 59.5%) and suitable eliminated half-life time ( T1/2 = 2.06 h), suggesting that 9u may be a potent candidate for treating acute myelogenous leukemia.
- Published
- 2019
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