Evidence map›Paper›PMID 32351597›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2020

The Mechanisms of the Herbal Components of CRSAS on HK-2 Cells in a Hypoxia/Reoxygenation Model Based on Network Pharmacology.

Naijing Ye, Dengpiao Xie, Bing Yang, Mingquan Li

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Article in Evidence-based complementary and alternative medicine : eCAM, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

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5citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Naijing YeHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Dengpiao XieHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Bing YangSichuan 2nd Hospital of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Mingquan LiHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.ORCID https://orcid.org/0000-0003-2867-4915

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury is a global problem, which brings a great burden to the society and family. The component of rhubarb,

objectiveTo assess the effect of CRSAS on human renal tubular epithelial cells (HK-2) after the hypoxia/reoxygenation (H/R) and investigate the potential mechanisms.

methodsNetwork pharmacology was used to predict the potential pathways shared by CRSAS and AKI. Cell counting kit-8 (CCK-8) was used to assess the HK-2 vitality. Apoptosis of HK-2 cells was detected by carboxyfluorescein succinimidyl ester/propidium iodide (CFSF/PI) staining. Expression of GRP78, CHOP, caspase-3, and Bax was detected by western blot and quantitative real-time RT-PCR.

resultCRSAS and AKI shared the endoplasmic reticulum stress (ERS) pathway based on network pharmacology analysis. CRSAS increases the vitality of HK-2 cells and reduces the apoptosis of HK-2 cells induced by H/R injury. The expression of GRP78 and CHOP in CRSAS groups was lower than that of control groups.

conclusionsH/R can induce HK-2 cell apoptosis and ERS. CRSAS can reduce HK-2 cell apoptosis by inhibiting the ERS. Therefore, CRSAS might be able to treat kidney disease due to I/R injury. Animal experiment should be done to further prove our finding.

Identifiers

PMID32351597
PMCPMC7174917

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