Feng Zhao

Prof. Dr. Feng Zhao

orcid

Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 October 2015 in Inflammation
Verified
Journal Article
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XJXin Jin
Xin Jin
JWJing Wang
Jing Wang
ZXZi-Ming Xia
Zi-Ming Xia
CSChang-Hui Shang
Chang-Hui Shang
QCQiu-Li Chao
Qiu-Li Chao
FZFeng Zhao
Feng Zhao

1 May 2019 in Phytomedicine
Verified
Journal Article
Closed access
HFHuaying Fan
Huaying Fan
ZGZhenfang Gao
Zhenfang Gao
KJKai Ji
Kai Ji
XLXin Li
Xin Li
JWJingbao Wu
Jingbao Wu
FZFeng Zhao
Feng Zhao

24 March 2014 in Journal of Natural Products
Verified
Journal Article
Closed access
ZLZhi-Guo Liu
Zhi-Guo Liu
ZLZhan-Lin Li
Zhan-Lin Li
JBJiao Bai
Jiao Bai
DMDa-Li Meng
Da-Li Meng
NLNing Li
Ning Li
HHHui-Ming Hua
Hui-Ming Hua

1 June 2021 in Current Medicinal Chemistry
Verified
Journal Article
Closed access
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MSMuhammad Sohail
Muhammad Sohail
WGWenna Guo
Wenna Guo
ZLZhiyong Li
Zhiyong Li
HXHui XU
Hui XU
FZFeng Zhao
Feng Zhao
FFFenghua Fu
Fenghua Fu
In recent years, due to the shortcomings of conventional chemotherapy, such as poor bioavailability, low treatment index, and unclear side effects, the focus of cancer research has shifted to new nanocarriers of chemotherapeutic drugs. By using biodegradable materials, nanocarriers generally have the advantages of good biocompatibility, low side effects, targeting, controlled release profile, and improved efficacy. More to the point, nanocarrier based anti-cancer drug delivery systems clearly show the potential to overcome the problems associated with conventional chemotherapy. In order to promote the in-depth research and development in this field, we herein summarized and analyzed various nanocarrier based drug delivery systems for cancer therapy, including the concepts, types, characteristics, and preparation methods. The active and passive targeting mechanisms of cancer therapy were also included, along with a brief introduction of the research progress of nanocarriers used for anti-cancer drug delivery in the past decade.

1 September 2016 in Fitoterapia
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Journal Article
Closed access
FGFeng Guo
Feng Guo
ZLZhanlin Li
Zhanlin Li
XXXiangwei Xu
Xiangwei Xu
KWKaibo Wang
Kaibo Wang
MSMeili Shao
Meili Shao
JBJiao Bai
Jiao Bai

28 April 2016 in Experimental and Therapeutic Medicine
Verified
Journal Article
Open access
PDF file
XJXin Jin
Xin Jin
SSShiqing Song
Shiqing Song
JWJing Wang
Jing Wang
QZQingzhen Zhang
Qingzhen Zhang
FQFeng Qiu
Feng Qiu
FZFeng Zhao
Feng Zhao
In the present study, the in vivo anti-inflammatory activity of Agrimonia pilosa Ledeb (AP) ethanol extract was confirmed in experimental animal models, including xylene‑induced ear edema in mice and carrageenan‑induced paw edema in rats. Tiliroside, the major component of AP extract, was isolated and purified by high‑performance liquid chromatography. The anti-inflammatory mechanism of tiliroside was then examined using lipopolysaccharide (LPS)-activated RAW 264.7 macrophage cells. An MTT assay was used to determine cytotoxicity and a Griess assay was used to determine nitric oxide (NO) production. Concentration levels of tumor necrosis factor‑α (TNF‑α) and interleukin‑6 (IL‑6) were determined by enzyme‑linked immunosorbent assay. Protein expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase‑2 (COX‑2), phosphorylated (p)‑extracellular signal‑regulated kinase (ERK) 1/2, p‑c‑Jun N‑terminal kinases (JNK), p‑p38 and inhibitor of κB‑α were detected by western blot analysis. AP ethanol extract was revealed to inhibit xylene‑induced ear edema in mice and carrageenan‑induced paw edema in rats. Tiliroside significantly suppressed the overproduction of NO (P<0.01), but revealed no notable inhibition of the release of TNF‑α and IL‑6. In addition, tiliroside significantly downregulated the elevated expression levels of iNOS and COX‑2 induced by LPS (P<0.01). The phosphorylation of JNK and p38 proteins were also significantly inhibited (P<0.01), however, tiliroside exhibited no obvious inhibition on the phosphorylation of ERK 1/2 and the degradation of IκB‑α protein. In conclusion, the anti-inflammatory molecular mechanism of tiliroside may involve the downregulation of iNOS and COX‑2 protein expression levels, and the inactivation of mitogen-activated protein kinase (MAPK)/JNK, in addition to the MAPK/p38 signaling pathway.