Evidence map›Paper›PMID 37817209›Full record

ArticleChinese medicine2023

Isoforskolin modulates AQP4-SPP1-PIK3C3 related pathway for chronic obstructive pulmonary disease via cAMP signaling.

Haochang Lin, Sha Cheng, Songye Yang, Qian Zhang, Lueli Wang, Jiangya Li, Xinyue Zhang, Liju Liang, Xiaoqian Zhou, Furong Yang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Chinese medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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  5. [Therapeutic effects of natural products on animal models of chronic obstructive pulmonary disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    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

14 authors at 2 institutions in 1 country.

Haochang LinSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.ORCID http://orcid.org/0000-0002-1845-1294
Sha ChengSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Songye YangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Qian ZhangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Lueli WangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Jiangya LiSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Xinyue ZhangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Liju LiangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Xiaoqian ZhouSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Furong YangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China.
Jingfeng SongSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China. 462759891@qq.com.
Xue CaoSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China. dir1865@163.com.
Weimin YangSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China. ywmbessie@yeah.net.
Zhiying WengSchool of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, No. 1168, Chunrong West Road, Yuhua Street, Chenggong New Town, Kunming, 650500, China. weng_zy@sina.com.
Kunming Medical University · CNGuiyang Medical University · CN

Funding

Kunming Medical University Innovation Fundation 2021S127National Natural Science Foundation of China 81402991National Natural Science Foundation of China 81860012National Natural Science Foundation of China 81870037Natural Science Foundation of Yunnan Province 2015IC001
6 · The paper itself

Abstract

backgroundCyclic adenosine monophosphate (cAMP) levels are directly activated by adenylate cyclase (AC) and play an anti-inflammatory role in chronic obstructive pulmonary disease (COPD). Previously, we have shown that isoforskolin (ISOF) can effectively activate AC1 and AC2 in vitro, improve pulmonary ventilation and reduce the inflammatory response in COPD model rats, supporting that ISOF may be a potential drug for the prevention and treatment of COPD, but the mechanism has not been explored in detail.

methodsThe potential pharmacological mechanisms of ISOF against COPD were analyzed by network pharmacology and multi-omics based on pharmacodynamic study. To use specific agonists, inhibitors and/or SiRNA for gene regulation function studies, combined qPCR, WB were applied to detect changes in mRNA and protein expression of important targets PIK3C3, AKT, mTOR, SPP1 and AQP4 which related to ISOF effect on COPD. And the key inflammatory factors detected by ELISA.

resultsBioinformatics suggested that the anti-COPD pharmacological mechanism of ISOF was related to PI3K-AKT signaling pathway, and suggested target protein like PIK3C3, AQP4, SPP1, AKT, mTOR. Using the AQP4 inhibitor,or inhibiting SPP1 expression by siRNA-SPP1 could block the PIK3C3-AKT-mTOR pathway and ameliorate chronic inflammation. ISOF showed cAMP-promoting effect then suppressed AQP4 expression, together with decreased level of IL-1β, IL-6, and IL-8.

conclusionsThese findings demonstrate ISOF controlled the cAMP-regulated PIK3C3-AKT-mTOR pathway, thereby alleviating inflammatory development in COPD. The cAMP/AQP4/PIK3C3 axis also modulate Th17/Treg differentiation, revealed potential therapeutic targets for this disease.

Indexed as

Anti-inflammationAQP4-SPP1-PIK3C3 signalingcAMPCOPDISOF

Identifiers

PMID37817209
PMCPMC10566078
OpenAlexW4387478012

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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.