The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Effects of L-carnitine against oxidative stress in human hepatocytes: involvement of peroxisome proliferator-activated receptor alpha
Open accessAbstract
BACKGROUND: Excessive oxidative stress and lipid peroxidation have been demonstrated to play important roles in the production of liver damage. L-carnitine is a natural substance and acts as a carrier for fatty acids across the inner mitochondrial membrane for subsequent beta-oxidation. It is also an antioxidant that reduces metabolic stress in the cells. Recent years L-carnitine has been proposed for treatment of various kinds of disease, including liver injury. This study was conducted to evaluate the protective effect of L-carnitine against hydrogen peroxide (H2O2)-induced cytotoxicity in a normal human hepatocyte cell line, HL7702. METHODS: We analyzed cytotoxicity using MTT assay and lactate dehydrogenase (LDH) release. Antioxidant activity and lipid peroxidation were estimated by reactive oxygen species (ROS) levels, activities and protein expressions of superoxide dismutase (SOD) and catalase (CAT), and malondialdehyde (MDA) formation. Expressions of peroxisome proliferator-activated receptor (PPAR)-alpha and its target genes were evaluated by RT-PCR or western blotting. The role of PPAR-alpha in L-carnitine-enhanced expression of SOD and CAT was also explored. Statistical analysis was performed by a one-way analysis of variance, and its significance was assessed by Dennett's post-hoc test. RESULTS: The results showed that L-carnitine protected HL7702 cells against cytotoxity induced by H2O2. This protection was related to the scavenging of ROS, the promotion of SOD and CAT activity and expression, and the prevention of lipid peroxidation in cultured HL7702 cells. The decreased expressions of PPAR-alpha, carnitine palmitoyl transferase 1 (CPT1) and acyl-CoA oxidase (ACOX) induced by H2O2 can be attenuated by L-carnitine. Besides, we also found that the promotion of SOD and CAT protein expression induced by L-carnitine was blocked by PPAR-alpha inhibitor MK886. CONCLUSIONS: Taken together, our findings suggest that L-carnitine could protect HL7702 cells against oxidative stress through the antioxidative effect and the regulation of PPAR-alpha also play an important part in the protective effect.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators
Issemann, I., & Green, S. (1990) · Nature · doi:10.1038/347645a0 · Cited by 3,519
Braissant, O., Foufelle, F., Scotto, C., Dauça, M., & Wahli, W. (1996) · Endocrinology · doi:10.1210/endo.137.1.8536636 · Cited by 2,217
The Mitochondrial Carnitine Palmitoyltransferase System — From Concept to Molecular Analysis
McGarry, J. D., & Brown, N. F. (1997) · European Journal of Biochemistry · doi:10.1111/j.1432-1033.1997.00001.x · Cited by 1,616 · cited 1×
“Therefore, mRNA expression of CPT1 and ACOX, two PPAR-a target genes that control fatty acid oxidation [30,31], were also investigated.”
Background
Cited by
Role of oxidative stress in the pathogenesis of nonalcoholic fatty liver disease
Chen, Z., Tian, R., She, Z., Cai, J., & Li, H. (2020) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2020.02.025 · Cited by 1,279
Nonalcoholic fatty liver disease (NAFLD) from pathogenesis to treatment concepts in humans
Pafili, K., & Roden, M. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2020.101122 · Cited by 330
Park, J. H., Vithayathil, S., Kumar, S., Sung, P.-L., Dobrolecki, L. E., Putluri, V., Bhat, V. B., Bhowmik, S. K., Gupta, V., Arora, K., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.02.004 · Cited by 313
Metadata
- Authors
- Li, J.-L., Wang, Q.-Y., Luan, H.-Y., Kang, Z.-C., & Wang, C.-B.
- Venue
- Journal of Biomedical Science
- Published
- 2012
- Volume
- 19
- Issue
- 1
- Pages
- 32
- ISSN
- 1021-7770 (ISSN-L)
- 1423-0127
- OpenAlex
- W2107283085
- Cited by
- 180
- References
- 3
- FWCI
- 9.12
- Type
- journal article
- Language
- en
- Open access
- diamond
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Effects of L-carnitine against oxidative stress in human hepatocytes: involvement of peroxisome proliferator-activated receptor alpha. https://app.cochat.ai/papers/10.1186/1423-0127-19-32
- The paper
- Li, J.-L., Wang, Q.-Y., Luan, H.-Y., Kang, Z.-C., & Wang, C.-B. (2012). Effects of L-carnitine against oxidative stress in human hepatocytes: involvement of peroxisome proliferator-activated receptor alpha. Journal of Biomedical Science. https://doi.org/10.1186/1423-0127-19-32
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.