Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux

Rui Chen; Xiaogang Gao; Lei Zhang; Wenyu Zhao; Li Zeng; Youhua Zhu; Zhiren Fu

doi:doi:10.11648/j.ijcems.20180403.15

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Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux

Rui Chen, Xiaogang Gao, Lei Zhang, Wenyu Zhao, Li Zeng, Youhua Zhu, Zhiren Fu

Published in International Journal of Clinical and Experimental Medical Sciences (Volume 4, Issue 3)

Received: 21 June 2018 Accepted: 2 August 2018 Published: 31 August 2018

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Abstract

Objective: This work was designed to investigate the protection of cannabidiol (CBD) against palmitic acid (PA)-induced injury in cultured hepatocytes and the underlying mechanism associated with autophagic flux. Methods: Experiment 1: Primary cultured hepatocytes were stimulated with PA (800 μmol/L) and treated with CBD (5 μmol/L) and chloroquine (CQ, 50 nmol/L) or not for 24 hours (1: control group; 2: PA-stimulated group; 3: PA-stimulated group treated with CBD; 4: PA-stimulated group treated with CBD and CQ). Autophagic flux was evaluated by Western blot analysis. Apoptosis was measured by flow cytometry. The mRNA expression of genes involved in endoplasmic reticulum stress was determined by reverse transcription PCR. The mitochondrial function was determined by using fluorescent probe including Rh123 and lucigenin. Experiment 2: Primary cultured hepatocytes were treated with CBD alone for 24 h (1: control group; 2: lower-dose CBD-treated group; 3: higher-dose CBD-treated group). Then, the autophagic flux was evaluated by Western blot analysis. Results: When compared to control group, exposure to PA significantly led to impaired autopagic flux (evidenced by increased ratio of LC3-II/LC3-I and protein expression of p62), increased apoptosis, endoplasmic reticulum stress (evidenced by increased mRNA expression of C/EBP homologous protein, glucose-regulated protein 78, and X-box protein 1), and mitochondrial dysfunction (evidenced by reduced mitochondrial membrane potential and enhanced formation of mitochondrial reactive oxygen species). When compared to PA-stimulated group, CBD treatment significantly attenuated PA-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes. The protection of CBD against PA was abolished by co-incubation with CQ. In addition, treatment with CBD alone had no significant effect on autophagic flux in cultured hepatocytes Conclusion: Cannabidiol attenuates palmitic acid-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes through promoting autophagic flux.

Published in	International Journal of Clinical and Experimental Medical Sciences (Volume 4, Issue 3)
DOI	10.11648/j.ijcems.20180403.15
Page(s)	51-56
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Cannabidiol, Palmitic Acid, Autophagic Flux, Hepatocytes, Apoptosis, Mitochondrial Dysfunction, Endoplasmic Reticulum Stress

References

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APA Style

Rui Chen, Xiaogang Gao, Lei Zhang, Wenyu Zhao, Li Zeng, et al. (2018). Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. International Journal of Clinical and Experimental Medical Sciences, 4(3), 51-56. https://doi.org/10.11648/j.ijcems.20180403.15

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ACS Style

Rui Chen; Xiaogang Gao; Lei Zhang; Wenyu Zhao; Li Zeng, et al. Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. Int. J. Clin. Exp. Med. Sci. 2018, 4(3), 51-56. doi: 10.11648/j.ijcems.20180403.15

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AMA Style

Rui Chen, Xiaogang Gao, Lei Zhang, Wenyu Zhao, Li Zeng, et al. Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. Int J Clin Exp Med Sci. 2018;4(3):51-56. doi: 10.11648/j.ijcems.20180403.15

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@article{10.11648/j.ijcems.20180403.15,
  author = {Rui Chen and Xiaogang Gao and Lei Zhang and Wenyu Zhao and Li Zeng and Youhua Zhu and Zhiren Fu},
  title = {Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux},
  journal = {International Journal of Clinical and Experimental Medical Sciences},
  volume = {4},
  number = {3},
  pages = {51-56},
  doi = {10.11648/j.ijcems.20180403.15},
  url = {https://doi.org/10.11648/j.ijcems.20180403.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20180403.15},
  abstract = {Objective: This work was designed to investigate the protection of cannabidiol (CBD) against palmitic acid (PA)-induced injury in cultured hepatocytes and the underlying mechanism associated with autophagic flux. Methods: Experiment 1: Primary cultured hepatocytes were stimulated with PA (800 μmol/L) and treated with CBD (5 μmol/L) and chloroquine (CQ, 50 nmol/L) or not for 24 hours (1: control group; 2: PA-stimulated group; 3: PA-stimulated group treated with CBD; 4: PA-stimulated group treated with CBD and CQ). Autophagic flux was evaluated by Western blot analysis. Apoptosis was measured by flow cytometry. The mRNA expression of genes involved in endoplasmic reticulum stress was determined by reverse transcription PCR. The mitochondrial function was determined by using fluorescent probe including Rh123 and lucigenin. Experiment 2: Primary cultured hepatocytes were treated with CBD alone for 24 h (1: control group; 2: lower-dose CBD-treated group; 3: higher-dose CBD-treated group). Then, the autophagic flux was evaluated by Western blot analysis. Results: When compared to control group, exposure to PA significantly led to impaired autopagic flux (evidenced by increased ratio of LC3-II/LC3-I and protein expression of p62), increased apoptosis, endoplasmic reticulum stress (evidenced by increased mRNA expression of C/EBP homologous protein, glucose-regulated protein 78, and X-box protein 1), and mitochondrial dysfunction (evidenced by reduced mitochondrial membrane potential and enhanced formation of mitochondrial reactive oxygen species). When compared to PA-stimulated group, CBD treatment significantly attenuated PA-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes. The protection of CBD against PA was abolished by co-incubation with CQ. In addition, treatment with CBD alone had no significant effect on autophagic flux in cultured hepatocytes Conclusion: Cannabidiol attenuates palmitic acid-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes through promoting autophagic flux.},
 year = {2018}
}

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TY  - JOUR
T1  - Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux
AU  - Rui Chen
AU  - Xiaogang Gao
AU  - Lei Zhang
AU  - Wenyu Zhao
AU  - Li Zeng
AU  - Youhua Zhu
AU  - Zhiren Fu
Y1  - 2018/08/31
PY  - 2018
N1  - https://doi.org/10.11648/j.ijcems.20180403.15
DO  - 10.11648/j.ijcems.20180403.15
T2  - International Journal of Clinical and Experimental Medical Sciences
JF  - International Journal of Clinical and Experimental Medical Sciences
JO  - International Journal of Clinical and Experimental Medical Sciences
SP  - 51
EP  - 56
PB  - Science Publishing Group
SN  - 2469-8032
UR  - https://doi.org/10.11648/j.ijcems.20180403.15
AB  - Objective: This work was designed to investigate the protection of cannabidiol (CBD) against palmitic acid (PA)-induced injury in cultured hepatocytes and the underlying mechanism associated with autophagic flux. Methods: Experiment 1: Primary cultured hepatocytes were stimulated with PA (800 μmol/L) and treated with CBD (5 μmol/L) and chloroquine (CQ, 50 nmol/L) or not for 24 hours (1: control group; 2: PA-stimulated group; 3: PA-stimulated group treated with CBD; 4: PA-stimulated group treated with CBD and CQ). Autophagic flux was evaluated by Western blot analysis. Apoptosis was measured by flow cytometry. The mRNA expression of genes involved in endoplasmic reticulum stress was determined by reverse transcription PCR. The mitochondrial function was determined by using fluorescent probe including Rh123 and lucigenin. Experiment 2: Primary cultured hepatocytes were treated with CBD alone for 24 h (1: control group; 2: lower-dose CBD-treated group; 3: higher-dose CBD-treated group). Then, the autophagic flux was evaluated by Western blot analysis. Results: When compared to control group, exposure to PA significantly led to impaired autopagic flux (evidenced by increased ratio of LC3-II/LC3-I and protein expression of p62), increased apoptosis, endoplasmic reticulum stress (evidenced by increased mRNA expression of C/EBP homologous protein, glucose-regulated protein 78, and X-box protein 1), and mitochondrial dysfunction (evidenced by reduced mitochondrial membrane potential and enhanced formation of mitochondrial reactive oxygen species). When compared to PA-stimulated group, CBD treatment significantly attenuated PA-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes. The protection of CBD against PA was abolished by co-incubation with CQ. In addition, treatment with CBD alone had no significant effect on autophagic flux in cultured hepatocytes Conclusion: Cannabidiol attenuates palmitic acid-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes through promoting autophagic flux.
VL  - 4
IS  - 3
ER  -

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Author Information

Rui Chen

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Xiaogang Gao

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Lei Zhang

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Wenyu Zhao

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Li Zeng

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Youhua Zhu

Organ Transplantation Center, Changhai Hospital of Naval Medical University, Shanghai, China
Zhiren Fu

Organ Transplantation Center, Changzheng Hospital of Naval Medical University, Shanghai, China

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APA Style

Rui Chen, Xiaogang Gao, Lei Zhang, Wenyu Zhao, Li Zeng, et al. (2018). Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. International Journal of Clinical and Experimental Medical Sciences, 4(3), 51-56. https://doi.org/10.11648/j.ijcems.20180403.15

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ACS Style

Rui Chen; Xiaogang Gao; Lei Zhang; Wenyu Zhao; Li Zeng, et al. Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. Int. J. Clin. Exp. Med. Sci. 2018, 4(3), 51-56. doi: 10.11648/j.ijcems.20180403.15

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AMA Style

Rui Chen, Xiaogang Gao, Lei Zhang, Wenyu Zhao, Li Zeng, et al. Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux. Int J Clin Exp Med Sci. 2018;4(3):51-56. doi: 10.11648/j.ijcems.20180403.15

Copy | Download

@article{10.11648/j.ijcems.20180403.15,
  author = {Rui Chen and Xiaogang Gao and Lei Zhang and Wenyu Zhao and Li Zeng and Youhua Zhu and Zhiren Fu},
  title = {Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux},
  journal = {International Journal of Clinical and Experimental Medical Sciences},
  volume = {4},
  number = {3},
  pages = {51-56},
  doi = {10.11648/j.ijcems.20180403.15},
  url = {https://doi.org/10.11648/j.ijcems.20180403.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20180403.15},
  abstract = {Objective: This work was designed to investigate the protection of cannabidiol (CBD) against palmitic acid (PA)-induced injury in cultured hepatocytes and the underlying mechanism associated with autophagic flux. Methods: Experiment 1: Primary cultured hepatocytes were stimulated with PA (800 μmol/L) and treated with CBD (5 μmol/L) and chloroquine (CQ, 50 nmol/L) or not for 24 hours (1: control group; 2: PA-stimulated group; 3: PA-stimulated group treated with CBD; 4: PA-stimulated group treated with CBD and CQ). Autophagic flux was evaluated by Western blot analysis. Apoptosis was measured by flow cytometry. The mRNA expression of genes involved in endoplasmic reticulum stress was determined by reverse transcription PCR. The mitochondrial function was determined by using fluorescent probe including Rh123 and lucigenin. Experiment 2: Primary cultured hepatocytes were treated with CBD alone for 24 h (1: control group; 2: lower-dose CBD-treated group; 3: higher-dose CBD-treated group). Then, the autophagic flux was evaluated by Western blot analysis. Results: When compared to control group, exposure to PA significantly led to impaired autopagic flux (evidenced by increased ratio of LC3-II/LC3-I and protein expression of p62), increased apoptosis, endoplasmic reticulum stress (evidenced by increased mRNA expression of C/EBP homologous protein, glucose-regulated protein 78, and X-box protein 1), and mitochondrial dysfunction (evidenced by reduced mitochondrial membrane potential and enhanced formation of mitochondrial reactive oxygen species). When compared to PA-stimulated group, CBD treatment significantly attenuated PA-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes. The protection of CBD against PA was abolished by co-incubation with CQ. In addition, treatment with CBD alone had no significant effect on autophagic flux in cultured hepatocytes Conclusion: Cannabidiol attenuates palmitic acid-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes through promoting autophagic flux.},
 year = {2018}
}

Copy | Download

TY  - JOUR
T1  - Cannabidiol Attenuates Palmitic Acid-Induced Injury in Cultured Hepatocytes Through Promoting Autophagic Flux
AU  - Rui Chen
AU  - Xiaogang Gao
AU  - Lei Zhang
AU  - Wenyu Zhao
AU  - Li Zeng
AU  - Youhua Zhu
AU  - Zhiren Fu
Y1  - 2018/08/31
PY  - 2018
N1  - https://doi.org/10.11648/j.ijcems.20180403.15
DO  - 10.11648/j.ijcems.20180403.15
T2  - International Journal of Clinical and Experimental Medical Sciences
JF  - International Journal of Clinical and Experimental Medical Sciences
JO  - International Journal of Clinical and Experimental Medical Sciences
SP  - 51
EP  - 56
PB  - Science Publishing Group
SN  - 2469-8032
UR  - https://doi.org/10.11648/j.ijcems.20180403.15
AB  - Objective: This work was designed to investigate the protection of cannabidiol (CBD) against palmitic acid (PA)-induced injury in cultured hepatocytes and the underlying mechanism associated with autophagic flux. Methods: Experiment 1: Primary cultured hepatocytes were stimulated with PA (800 μmol/L) and treated with CBD (5 μmol/L) and chloroquine (CQ, 50 nmol/L) or not for 24 hours (1: control group; 2: PA-stimulated group; 3: PA-stimulated group treated with CBD; 4: PA-stimulated group treated with CBD and CQ). Autophagic flux was evaluated by Western blot analysis. Apoptosis was measured by flow cytometry. The mRNA expression of genes involved in endoplasmic reticulum stress was determined by reverse transcription PCR. The mitochondrial function was determined by using fluorescent probe including Rh123 and lucigenin. Experiment 2: Primary cultured hepatocytes were treated with CBD alone for 24 h (1: control group; 2: lower-dose CBD-treated group; 3: higher-dose CBD-treated group). Then, the autophagic flux was evaluated by Western blot analysis. Results: When compared to control group, exposure to PA significantly led to impaired autopagic flux (evidenced by increased ratio of LC3-II/LC3-I and protein expression of p62), increased apoptosis, endoplasmic reticulum stress (evidenced by increased mRNA expression of C/EBP homologous protein, glucose-regulated protein 78, and X-box protein 1), and mitochondrial dysfunction (evidenced by reduced mitochondrial membrane potential and enhanced formation of mitochondrial reactive oxygen species). When compared to PA-stimulated group, CBD treatment significantly attenuated PA-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes. The protection of CBD against PA was abolished by co-incubation with CQ. In addition, treatment with CBD alone had no significant effect on autophagic flux in cultured hepatocytes Conclusion: Cannabidiol attenuates palmitic acid-induced impaired autophagic flux, apoptosis, endoplasmic reticulum stress, and mitochondrial dysfunction in cultured hepatocytes through promoting autophagic flux.
VL  - 4
IS  - 3
ER  -

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