ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Protective Effects of Gallic Acid Against NiSO4-Induced Toxicity Through Down-Regulation of the Ras/ERK Signaling Pathway in Beas-2B Cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Deciphering the cancer chemopreventive potential of phytochemicals: an integrative perspective on molecular targets and signaling networks.Cancer cell international · 2026Review
- Anti-nephrotoxic, antioxidant and anti-inflammatory efficiency ofOpen veterinary journal · 2025Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Gallic Acid Attenuates Postoperative Intra-Abdominal Adhesion by Inhibiting Inflammatory Reaction in a Rat Model.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND This study aimed to explore the preventive effects of gallic acid (GA) on the toxicity induced by NiSO4 in Beas-2B cells. MATERIAL AND METHODS Beas-2B cell viability was measured by MTT assay. The degree of oxidative stress was detected by measuring the levels of reactive oxygen species (ROS) and lipid peroxide (LPO). The rate of apoptosis was measured by flow cytometry. Ras/ERK-related protein levels were analyzed by Western blot analysis, which including Ras, ERK, c-Myc, PARP, and PARP cleavage. RESULTS MTT assay showed that NiSO4 induced cytotoxicity, while GA had a protective role against toxicity. Additionally, GA could reduce the apoptotic cell number and the level of ROS in Beas-2B cells induced by NiSO4. Western blot analysis demonstrated that NiSO4 could up-regulate the related protein in the Ras/ERK signaling pathway. Furthermore, we observed that GA could alleviate the toxicity of NiSO4 through regulating protein changes in the Ras/ERK signaling pathway. CONCLUSIONS Preventive effects of GA on NiSO4-induced cytotoxicity in Beas-2B cells may be through the Ras/ERK signaling pathways.
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Registered trials
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.