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Your search keyword '"Li, Hongliang"' showing total 13 results
Start Over Author "Li, Hongliang" Publication Year Range Last 10 years Publisher hindawi limited
13 results on '"Li, Hongliang"'

1. The Dectin-1 Receptor Signaling Pathway Mediates the Remyelination Effect of Lentinan through Suppression of Neuroinflammation and Conversion of Microglia

Author

Zhang, Dandan, primary, Jia, Yue, additional, Sun, Xingzong, additional, Li, Haoran, additional, Yin, Min, additional, Li, Hongliang, additional, Dai, Lili, additional, Han, Li, additional, Wang, Lei, additional, Qian, Menghan, additional, Du, Jing, additional, Zhu, Keming, additional, and Bao, Hongkun, additional

Published
2022
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6. Perioperative Circulating Tumor Cells (CTCs), MCTCs, and CTC-White Blood Cells Detected by a Size-Based Platform Predict Prognosis in Renal Cell Carcinoma

Author

Wang, Zhenlong, primary, Zhang, Peng, additional, Chong, Yue, additional, Xue, Yuquan, additional, Yang, Xiaojie, additional, Li, Hecheng, additional, Wang, Li, additional, Zhang, Yaping, additional, Chen, Qi, additional, Li, Zhaolun, additional, Xue, Li, additional, Li, HongLiang, additional, and Chong, Tie, additional

Published
2021
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7. Kaempferia parviflora and Its Methoxyflavones: Chemistry and Biological Activities

Author

Chen, Dalin, Li, Hongliang, Li, Wen, Feng, Shuo, and Deng, Dingsen

Subjects
0301 basic medicine, Kaempferia parviflora, ved/biology, Chemistry, ved/biology.organism_classification_rank.species, Review Article, lcsh:Other systems of medicine, Pharmacology, lcsh:RZ201-999, Neuroprotection, Bioavailability, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Complementary and alternative medicine, 030220 oncology & carcinogenesis, Transdermal
Abstract

Kaempferia parviflora (KP), a health-promoting herb, has been traditionally used for treating a variety of diseases. Pharmacological studies have claimed the various benefits from KP and its main effective methoxyflavones, including cellular metabolism-regulating activity, anticancer activity, vascular relaxation and cardioprotective activity, sexual enhancing activity, neuroprotective activity, antiallergic, anti-inflammatory, and antioxidative activity, antiosteoarthritis activity, antimicroorganism activity, and transdermal permeable activity. These might be associated with increased mitochondrial functions and activated cGMP-NO signaling pathway. However, the underlying molecular mechanisms of KP and its methoxyflavones are still under investigation. The clinical applications of KP and its methoxyflavones may be limited due to their low bioavailability. But promising strategies are on the way. This review will comprehensively discuss the biological activities of KP and its methoxyflavones.

Published
2018

13. The vasorelaxant effect of antidiabetic drug nateglinide via activation of voltage‐dependent K+ channels in aortic smooth muscle.

Author

Li, Hongliang, Kim, Hye Won, Shin, Sung Eun, Seo, Mi Seon, An, Jin Ryeol, Jung, Won‐Kyo, Ha, Kwon‐Soo, Han, Eun‐Taek, Hong, Seok‐Ho, Bang, Hyoweon, Choi, Il‐Whan, Na, Sung Hun, and Park, Won Sun

Subjects
*HYPOGLYCEMIC agents, *SMOOTH muscle, *PHENYLEPHRINE, *AORTA, *PAXILLINE
Abstract

Summary: Aims: We investigated the vasorelaxant effect of nateglinide and its related mechanisms using phenylephrine (Phe)‐induced precontracted aortic rings. Methods: Arterial tone measurement was performed in aortic smooth muscle. Results: The application of nateglinide induced vasorelaxation in a concentration‐dependent manner. Pretreatment with the large‐conductance Ca2+‐activated K+ (BKCa) channel inhibitor paxilline, the inwardly rectifying K+ (Kir) channel inhibitor Ba2+, and ATP‐sensitive K+ (KATP) channel inhibitor glibenclamide did not affect the vasorelaxant effect of nateglinide. However, pretreatment with the voltage‐dependent K+ (Kv) channel inhibitor 4‐aminopyridine (4‐AP) effectively reduced the vasorelaxant effect of nateglinide. Pretreatment with the Ca2+ inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca2+‐ATPase inhibitor thapsigargin did not change the vasorelaxant effect of nateglinide. Additionally, the vasorelaxant effect of nateglinide was not altered in the presence of an adenylyl cyclase, a protein kinase A, a guanylyl cyclase, or a protein kinase G inhibitor. The vasorelaxant effect of nateglinide was not affected by the elimination of the endothelium. In addition, pretreatment with a nitric oxide synthase inhibitor, L‐NAME, and a small‐conductance Ca2+‐activated K+ (SKCa) channel inhibitor, apamin, did not change the vasorelaxant effect of nateglinide. Conclusion: Nateglinide induced vasorelaxation via the activation of the Kv channel independent of other K+ channels, Ca2+ channels, intracellular Ca2+ ([Ca2+]i), and the endothelium. [ABSTRACT FROM AUTHOR]

Published
2018
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