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14 results on '"Ran, Zhaojin"'

9. Effect of a newly synthesized compound on delaying pre-harvest sprouting in winter wheat (Triticum aestivum L.)

Author

Hou Xinxin, Mao Zhiqiang, Tingting Wei, Ran Zhaojin, Xin Xuecheng, Cui Shunyan, and Zhou Fan

Subjects
0106 biological sciences, 0301 basic medicine, Methyl jasmonate, Physiology, Dimethyl sulfoxide, food and beverages, Plant physiology, Plant Science, 01 natural sciences, 03 medical and health sciences, chemistry.chemical_compound, Horticulture, 030104 developmental biology, chemistry, Germination, Gibberellin, Agronomy and Crop Science, Abscisic acid, Acetamide, 010606 plant biology & botany, Sprouting
Abstract

Pre-harvest sprouting (PHS) of wheat commonly occurs in rainy or humid weather conditions before harvest. It not only affects the yield but also decreases the wheat quality and seed value. As the most important grain crop in the world, reducing PHS and improving the yield and quality of wheat is essential. In this study, a new compound of methyl jasmonate (MeJA) analog, N-(2, 4-dimethoxyphenyl)-2-(3-oxo-2-pentylcyclopentyl) acetamide, was synthesized and its effect on PHS tested. Concentration screening of the new compound showed that [1500 mg L−1 N-(2, 4-dimethoxyphenyl)-2-(3-oxo-2-pentylcyclopentyl) acetamide + 1% dimethyl sulfoxide (DMSO) + 0.1% penetrant (T2)] was suitable for inhibiting PHS. Exogenously applied T2 effectively inhibited seed germination and increased abscisic acid (ABA) and decreased gibberellin (GA) concentration. These changes in endogenous hormones led to a significant reduction in α-amylase activity. The results of RNA-Seq and quantitative real-time PCR indicated that expression of genes encoding biosynthesis and catabolism of ABA, GA and α-amylase had a consistent trend with the results of hormone concentrations and α-amylase activity. In conclusion, application of T2 can delay PHS by 2 to 3 days through changing of endogenous hormones to significantly decrease the α-amylase activity and ensure the vigor of wheat seed. These findings can provide some help for the development of a retardant to prevent PHS.

Published
2021

10. Computational Analysis on Antioxidant Activity of Four Characteristic Structural Units from Persimmon Tannin.

Author

Wang, Zhongmin, Liu, Zhigao, Wu, Chenxi, Liu, Songlin, Wang, Dianhui, Hu, Chaohao, Chen, Tao, Ran, Zhaojin, Gan, Weijiang, and Li, Guiyin

Subjects
TANNINS, ANTIOXIDANT analysis, FRONTIER orbitals, MOLECULAR structure, ANALYTICAL chemistry, ABSTRACTION reactions
Abstract

Antioxidants are molecules that can prevent the harmful effects of oxygen, help capture and neutralize free radicals, and thus eliminate the damage of free radicals to the human body. Persimmon tannin (PT) has excellent antioxidant activity, which is closely related to its molecular structure. We report here a comparative study of four characteristic structural units from PT (epicatechin gallate (ECG), epigallocatechin gallate (EGCG), A−type linked ECG dimer (A−ECG dimer), A−type linked EGCG dimer (A−EGCG dimer)) to explore the structure–activity relationship by using the density functional theory. Based on the antioxidation mechanism of hydrogen atom transfer, the most favorable active site for each molecule exerts antioxidant activity is determined. The structural parameters, molecular electrostatic potential, and frontier molecular orbital indicate that the key active sites are located on the phenolic hydroxyl group of the B ring for ECG and EGCG monomers, and the key active sites of the two dimers are located on the phenolic hydroxyl groups of the A and D' rings. The natural bond orbital and bond dissociation energy of the phenolic hydroxyl hydrogen atom show that the C11−OH in the ECG monomer and the C12−OH in the EGCG monomer are the most preferential sites, respectively. The most active site of the two A−linked dimers is likely located on the D' ring C20′ phenolic hydroxyl group. Based on computational analysis of quantum chemical parameters, the A−ECG dimer is a more potent antioxidant than the A−EGCG dimer, ECG, and EGCG. This computational analysis provides the structure–activity relationship of the four characteristic units which will contribute to the development of the application of PT antioxidants in the future. [ABSTRACT FROM AUTHOR]

Published
2023
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11. 2,4,5-Trichloro-6-((2,4,6-trichlorophenyl)amino)isophthalonitrile, Exerts Anti-bladder Activities through IGF-1R/STAT3 Signaling

Author

He Lin, Chai Baoshan, Wang Wanqiu, Wang Yunhua, Bi Yi, Guang Haihong, Jiao Jiayuan, Ran Zhaojin, and Bu Yanxin

Subjects
STAT3 Transcription Factor, MAPK/ERK pathway, Cell Survival, medicine.medical_treatment, Urinary Bladder, Antineoplastic Agents, Apoptosis, 010402 general chemistry, 01 natural sciences, Cell Line, Receptor, IGF Type 1, Cell Line, Tumor, Nitriles, Drug Discovery, medicine, Humans, Cytotoxic T cell, Cytotoxicity, 010405 organic chemistry, Chemistry, Kinase, Growth factor, Cell Cycle, Receptors, Somatomedin, General Chemistry, General Medicine, Cell cycle, Molecular biology, 0104 chemical sciences, Molecular Docking Simulation, Urinary Bladder Neoplasms, STAT protein, Signal Transduction
Abstract

2,4,5-Trichloro-6-((2,4,6-trichlorophenyl)amino)isophthalonitrile (SYD007) is a small molecule compound that was synthesized according to the structure of diarylamine. In this study, we evaluated the anti-bladder activities of SYD007, and determined its cytotoxic mechanism. We found that SYD007 exerted cytotoxicity to bladder cancer cells. Furthermore, SYD007 induced bladder cancer cell early apoptosis and arrested cell cycle. Mechanistically, SYD007 suppressed phosphorylated signal transducer and activator of transcription 3 (p-STAT3) (Tyr705) level in parallel with increases of p-extracellular signal-regulated kinase (ERK) and p-AKT. SYD007 significantly inhibited insulin-like growth factor 1 (IGF-1)-induced STAT3 activation through down-regulation of total IGF-1R level. No dramatic changes in IGF-1R mRNA levels were observed in SYD007-treated cells, suggesting that SYD007 acted primarily at a posttranscriptional level. Using molecular docking analysis, SYD007 was identified as an IGF-1R inhibitor. In summary, we reported that SYD007 exerted anti-bladder activities, and these effects were partially due to inhibition of IGF-1R/STAT3 signaling.

Published
2019

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