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Phytochemistry and pharmacology of natural prenylated flavonoids
Hua-Wei Lv,Qiao-Liang Wang,Meng Luo,Meng-Di Zhu,Hui-Min Liang,Wen-Jing Li,Hai Cai,Zhong-Bo Zhou,Hong Wang,Sheng-Qiang Tong,Xing-Nuo Li 대한약학회 2023 Archives of Pharmacal Research Vol.46 No.4
Prenylated flavonoids are a special kind of flavonoid derivative possessing one or more prenyl groups in the parent nucleus of the flavonoid. The presence of the prenyl side chain enriched the structural diversity of flavonoids and increased their bioactivity and bioavailability. Prenylated flavonoids show a wide range of biological activities, such as anti-cancer, anti-inflammatory, neuroprotective, anti-diabetic, anti-obesity, cardioprotective effects, and anti-osteoclastogenic activities. In recent years, many compounds with significant activity have been discovered with the continuous excavation of the medicinal value of prenylated flavonoids, and have attracted the extensive attention of pharmacologists. This review summarizes recent progress on research into natural active prenylated flavonoids to promote new discoveries of their medicinal value.
Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
Meng-Meng Lv,Ming-Hui Tan,Li-Wen Lu,Rong-Hua Zhang,Zhi-Yong Guo,Cheng-Xiong Liu,Jin Yang,Kun Zou,Peter Proksch 한국생약학회 2018 Natural Product Sciences Vol.24 No.3
Two new polyketides, chinoketides A and B (1 - 2) with a known compound xylarphthalide A (3), were isolated from the solid medium of the endophytes from the leaves of the relic plant Distylium chinense with the "black-box" co-culture method, and the structures of two new compounds were elucidated by NMR, MS and CD spectra. And the absolute configurations of chinoketides A (1) and B (2) were determined as 2R,3R,8S and 5R,6S by calculating their ECD spectra to compare with the experimental CD spectra. Finally, the antimicrobial activities were evaluated to Erwinia carotovora sub sp. Carotovora (Jones) Bersey et al, and the results showed that compounds 1 - 3 displayed the antimicrobial activities with MIC value at 20.5, 30.4 and 10.2 mg/mL.
Silencing IL-23 expression by a small hairpin RNA protects against asthma in mice
Li, Yanchun,Sun, Meng,Cheng, Huanji,Li, Shanyu,Liu, Li,Qiao, Hongmei,Hua, Shucheng,Lu, Jirong Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.4
To determine the impact of IL-23 knockdown by RNA interference on the development and severity of ovalbumin (OVA)-induced asthmatic inflammation, and the potential mechanisms in mice, the IL-23-specific RNAi-expressing pSRZsi-IL-23p19 plasmid was constructed and inhaled into OVA-sensitized mice before each challenge, as compared with that of control mice treated with alum or budesonide. Inhalation of the pSRZsi-IL-23p19, significantly reduced the levels of OVA-challenge induced IL-23 in the lung tissues by nearly 75%, determined by RT-PCR. In addition, knockdown of IL-23 expression dramatically reduced the numbers of eosinophils and neutrophils in BALF and mitigated inflammation in the lungs of asthmatic mice. Furthermore, knockdown of IL-23 expression significantly decreased the levels of serum IgE, IL-23, IL-17, and IL-4, but not IFN${\gamma}$, and its anti-inflammatory effects were similar to or better than that of treatment with budesonide in asthmatic mice. Our data support the notion that IL-23 and associated Th17 responses contribute to the pathogenic process of bronchial asthma. Knockdown of IL-23 by RNAi effectively inhibits asthmatic inflammation, which is associated with mitigating the production of IL-17 and IL-4 in asthmatic mice.
Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
Silencing IL-23 expression by a small hairpin RNA protects against asthma in mice
Yanchun Li,Shucheng Hua,Jirong Lu,Meng Sun,Huanji Cheng,Shanyu Li,Li Liu,Hongmei Qiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.4
To determine the impact of IL-23 knockdown by RNA interference on the development and severity of ovalbumin (OVA)-induced asthmatic inflammation, and the potential mechanisms in mice, the IL-23-specific RNAi-expressing pSRZsi-IL-23p19 plasmid was constructed and inhaled into OVA-sensitized mice before each challenge, as compared with that of control mice treated with alum or budesonide. Inhalation of the pSRZsi-IL-23p19, significantly reduced the levels of OVA-challenge induced IL-23 in the lung tissues by nearly 75%, determined by RT-PCR. In addition, knockdown of IL-23 expression dramatically reduced the numbers of eosinophils and neutrophils in BALF and mitigated inflammation in the lungs of asthmatic mice. Furthermore, knockdown of IL-23 expression significantly decreased the levels of serum IgE, IL-23,IL-17, and IL-4, but not IFNγ, and its anti-inflammatory effects were similar to or better than that of treatment with budesonide in asthmatic mice. Our data support the notion that IL-23 and associated Th17 responses contribute to the pathogenic process of bronchial asthma. Knockdown of IL-23 by RNAi effectively inhibits asthmatic inflammation, which is associated with mitigating the production of IL-17 and IL-4 in asthmatic mice.
Yao, Li-Hua,Wang, Jinxiu,Liu, Chao,Wei, Shanshan,Li, Guoyin,Wang, Songhua,Meng, Wei,Liu, Zhi-Bin,Huang, Li-Ping The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
Genetic Variations in TERT-CLPTM1L Genes and Risk of Lung Cancer in a Chinese Population
Zhao, Meng-Meng,Zhang, Yue,Shen, Li,Ren, Yang-Wu,Li, Xue-Lian,Yin, Zhi-Hua,Zhou, Bao-Sen Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.6
Background: This study was conducted to investigate the association between single nucleotide polymorphisms (SNPs) in telomerase reverse transcriptase (TERT) and cleft lip and palate transmembrane1-like (CLPTM1L) and lung cancer risk in a Chinese population. Methods: We performed a hospital-based case-control study, including 980 lung cancer cases and 1000 cancer-free controls matched for age and sex. Each case and control was interviewed to collect information by well-trained interviewers. A total of 5 ml of venous blood was collected for genotype testing of TERT rs2736098 and CLPTM1L rs401681 using TaqMan methodology. Results: The results revealed that the variant homozygote TERT rs2736098TT was associated with an increased risk of lung cancer (OR=2.017, 95%CI=1.518-2.681), especially lung adenocarcinoma (OR=2.117, 95%CI=1.557-3.043) and small cell carcinoma (OR=1.979, 95%CI: 1.174-3.334), compared with the TERT rs2736098CC genotype. Similar results were observed in non-smokers. Conclusion: The TERT rs2736098 polymorphism might affect the susceptibility to lung cancer in Chinese populations. The associations need to be verified in larger and different populations.