Evidence map›Paper›PMID 26040661›Full record

ArticlePharmaceutical research2015

Suppression of Remodeling Behaviors with Arachidonic Acid Modification for Enhanced in vivo Antiatherogenic Efficacies of Lovastatin-loaded Discoidal Recombinant High Density Lipoprotein.

Hongliang He, Mengyuan Zhang, Lisha Liu, Shuangshuang Zhang, Jianping Liu, Wenli Zhang

Abstract read
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In one paragraph

Article in Pharmaceutical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hongliang HeDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China.
Mengyuan ZhangDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China.
Lisha LiuDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China.
Shuangshuang ZhangDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China.
Jianping LiuDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China. jianpingliu1293@163.com.
Wenli ZhangDepartment of Pharmaceutics, China Pharmaceutical University, No.24, Tongjia Lane, Nanjing, 210009, People's Republic of China. jianpingliu1293@163.com.
China Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeA series of in vitro evaluation in our previous studies had proved that arachidonic acid (AA) modification could suppress the remodeling behaviors of lovastatin-loaded discoidal reconstituted high density lipoprotein (LT-d-rHDL) by restraining the reactivity with lecithin cholesterol acyltransferase (LCAT) for reducing undesired drug leakage. This study focuses on the investigation of AA-modified LT-d-rHDL (AA-LT-d-rHDL) in atherosclerotic New Zealand White (NZW) rabbit models to explore whether AA modification could enhance drug targeting delivery and improve antiatherogenic efficacies in vivo.

methodsAfter pharmacokinetics of AA-LT-d-rHDL modified with different AA amount were investigated in atherosclerotic NZW rabbits, atherosclerotic lesions targeting property was assessed by ex vivo imaging of aortic tree and drug distribution. Furthermore, their antiatherogenic efficacies were elaborately evaluated and compared by typical biochemical indices.

resultsWith AA modification amount augmenting, circulation time of AA-LT-d-rHDL was prolonged, and drug accumulation in the target locus was increased, eventually the significant appreciation in antiatherogenic efficacies were further supported by lower level of bad cholesterol, decreased atherosclerotic lesions areas and mean intima-media thickness (MIT), markedly attenuated matrix metalloproteinase-9 (MMP-9) protein expression and macrophage infiltration.

conclusionThis proof-of-concept study demonstrated that AA-LT-d-rHDL could enhance drug accumulation in atherosclerotic lesion and impede atherosclerosis progression more effectively.

Indexed as

AnimalsArachidonic AcidAtherosclerosisCholesterolDrug CarriersDrug Delivery SystemsLipoproteins, HDLLovastatinMacrophagesMaleMatrix Metalloproteinase 9Phosphatidylcholine-Sterol O-AcyltransferaseRabbitsArachidonic AcidCholesterolDrug CarriersLipoproteins, HDLLovastatinMatrix Metalloproteinase 9Phosphatidylcholine-Sterol O-Acyltransferaseantiatherogenic efficaciesarachidonic acid modified d-rHDLdrug leakageLCATremodeling behaviors

Identifiers

PMID26040661
OpenAlexW589865796

What OpenQuestion holds

Texttitle and abstract
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.