The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells

Yossi Dagon; Yosefa Avraham; Gabriela Link; Olga Zolotarev; Raphael Mechoulam; Elliot M. Berry

doi:10.1016/j.nbd.2007.04.017

The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells

Yossi Dagon
, Yosefa Avraham
, Gabriela Link
, Olga Zolotarev
, Raphael Mechoulam
, Elliot M. Berry^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

Diabetic neuropathy (DN) is a common complication of diabetes mellitus resulting in cognitive dysfunction and synaptic plasticity impairment. Hyperglycemia plays a critical role in the development and progression of DN, through a number of mechanisms including increased oxidative stress. Cannabinoids are a diverse family of compounds which can act as antioxidative agents and exhibit neuroprotective properties. We investigated the effect of the synthetic cannabinoid HU-210 on brain function of streptozotocin (STZ)-induced diabetic mice. These animals exhibit hyperglycemia, increased cerebral oxidative stress and impaired brain function. HU-210, through a receptor independent pathway, alleviates the oxidative damage and cognitive impairment without affecting glycemic control. To study the neuroprotective mechanism(s) involved, we cultured PC12 cells under hyperglycemic conditions. Hyperglycemia enhanced oxidative stress and cellular injuries were all counteracted by HU-210-in a dose dependent manner. These results suggest cannabinoids might have a therapeutic role in the management of the neurological complications of diabetes.

Original language	English
Pages (from-to)	174-181
Number of pages	8
Journal	Neurobiology of Disease
Volume	27
Issue number	2
DOIs	https://doi.org/10.1016/j.nbd.2007.04.017
State	Published - Aug 2007

Bibliographical note

Funding Information:
The research was supported by the Binational Science Foundation (BSF) and “Women’s Health” initiative of the Hadassah Medical Organization. We would like to thank Dr Lia Vorobiav and the students: Mayer Saidian, Rafael Mevorah and Reut Pienik for their technical assistance.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Access to Document

10.1016/j.nbd.2007.04.017

Cite this

@article{3a9d08789f974dadad59c978e8d0b0b7,

title = "The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells",

abstract = "Diabetic neuropathy (DN) is a common complication of diabetes mellitus resulting in cognitive dysfunction and synaptic plasticity impairment. Hyperglycemia plays a critical role in the development and progression of DN, through a number of mechanisms including increased oxidative stress. Cannabinoids are a diverse family of compounds which can act as antioxidative agents and exhibit neuroprotective properties. We investigated the effect of the synthetic cannabinoid HU-210 on brain function of streptozotocin (STZ)-induced diabetic mice. These animals exhibit hyperglycemia, increased cerebral oxidative stress and impaired brain function. HU-210, through a receptor independent pathway, alleviates the oxidative damage and cognitive impairment without affecting glycemic control. To study the neuroprotective mechanism(s) involved, we cultured PC12 cells under hyperglycemic conditions. Hyperglycemia enhanced oxidative stress and cellular injuries were all counteracted by HU-210-in a dose dependent manner. These results suggest cannabinoids might have a therapeutic role in the management of the neurological complications of diabetes.",

author = "Yossi Dagon and Yosefa Avraham and Gabriela Link and Olga Zolotarev and Raphael Mechoulam and Berry, \{Elliot M.\}",

note = "Funding Information: The research was supported by the Binational Science Foundation (BSF) and “Women{\textquoteright}s Health” initiative of the Hadassah Medical Organization. We would like to thank Dr Lia Vorobiav and the students: Mayer Saidian, Rafael Mevorah and Reut Pienik for their technical assistance.",

year = "2007",

month = aug,

doi = "10.1016/j.nbd.2007.04.017",

language = "אנגלית",

volume = "27",

pages = "174--181",

journal = "Neurobiology of Disease",

issn = "0969-9961",

publisher = "Academic Press Inc.",

number = "2",

}

TY - JOUR

T1 - The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells

AU - Dagon, Yossi

AU - Avraham, Yosefa

AU - Link, Gabriela

AU - Zolotarev, Olga

AU - Mechoulam, Raphael

AU - Berry, Elliot M.

N1 - Funding Information: The research was supported by the Binational Science Foundation (BSF) and “Women’s Health” initiative of the Hadassah Medical Organization. We would like to thank Dr Lia Vorobiav and the students: Mayer Saidian, Rafael Mevorah and Reut Pienik for their technical assistance.

PY - 2007/8

Y1 - 2007/8

N2 - Diabetic neuropathy (DN) is a common complication of diabetes mellitus resulting in cognitive dysfunction and synaptic plasticity impairment. Hyperglycemia plays a critical role in the development and progression of DN, through a number of mechanisms including increased oxidative stress. Cannabinoids are a diverse family of compounds which can act as antioxidative agents and exhibit neuroprotective properties. We investigated the effect of the synthetic cannabinoid HU-210 on brain function of streptozotocin (STZ)-induced diabetic mice. These animals exhibit hyperglycemia, increased cerebral oxidative stress and impaired brain function. HU-210, through a receptor independent pathway, alleviates the oxidative damage and cognitive impairment without affecting glycemic control. To study the neuroprotective mechanism(s) involved, we cultured PC12 cells under hyperglycemic conditions. Hyperglycemia enhanced oxidative stress and cellular injuries were all counteracted by HU-210-in a dose dependent manner. These results suggest cannabinoids might have a therapeutic role in the management of the neurological complications of diabetes.

AB - Diabetic neuropathy (DN) is a common complication of diabetes mellitus resulting in cognitive dysfunction and synaptic plasticity impairment. Hyperglycemia plays a critical role in the development and progression of DN, through a number of mechanisms including increased oxidative stress. Cannabinoids are a diverse family of compounds which can act as antioxidative agents and exhibit neuroprotective properties. We investigated the effect of the synthetic cannabinoid HU-210 on brain function of streptozotocin (STZ)-induced diabetic mice. These animals exhibit hyperglycemia, increased cerebral oxidative stress and impaired brain function. HU-210, through a receptor independent pathway, alleviates the oxidative damage and cognitive impairment without affecting glycemic control. To study the neuroprotective mechanism(s) involved, we cultured PC12 cells under hyperglycemic conditions. Hyperglycemia enhanced oxidative stress and cellular injuries were all counteracted by HU-210-in a dose dependent manner. These results suggest cannabinoids might have a therapeutic role in the management of the neurological complications of diabetes.

UR - https://www.scopus.com/pages/publications/34447632664

U2 - 10.1016/j.nbd.2007.04.017

DO - 10.1016/j.nbd.2007.04.017

M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???

C2 - 17604177

AN - SCOPUS:34447632664

SN - 0969-9961

VL - 27

SP - 174

EP - 181

JO - Neurobiology of Disease

JF - Neurobiology of Disease

IS - 2

ER -

The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice and hyperglycemic pheochromocytoma PC12 cells

Abstract

Bibliographical note

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this