Effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells

Y Cao, X Li, P Shi, Lexin Wang, Z G Sui

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound.
Objective: To elucidate the protective effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs).
Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (??m) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of L-carnitine.
Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.
Original languageEnglish
Pages (from-to)123-130
Number of pages8
JournalPharmacology
Volume94
Issue number3-4
DOIs
Publication statusPublished - Nov 2014

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Retinal Ganglion Cells
Carnitine
Oxidative Stress
Glucose
Apoptosis
Lipid Peroxidation
Reactive Oxygen Species
Antioxidants
Bisbenzimidazole
Caspase 9
Mitochondrial Membrane Potential
Mitochondrial Membranes
Diabetic Retinopathy
Glutathione Peroxidase
Cytochromes c
Caspase 3
Catalase
Superoxide Dismutase
Down-Regulation
Western Blotting

Cite this

Cao, Y ; Li, X ; Shi, P ; Wang, Lexin ; Sui, Z G. / Effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells. In: Pharmacology. 2014 ; Vol. 94, No. 3-4. pp. 123-130.
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abstract = "Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound. Objective: To elucidate the protective effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs). Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (??m) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of L-carnitine. Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.",
keywords = "Apoptosis, Diabetic retinopathy, Glucose, L-Carnitine, Oxidative stress",
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Effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells. / Cao, Y; Li, X; Shi, P; Wang, Lexin; Sui, Z G.

In: Pharmacology, Vol. 94, No. 3-4, 11.2014, p. 123-130.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells

AU - Cao, Y

AU - Li, X

AU - Shi, P

AU - Wang, Lexin

AU - Sui, Z G

N1 - Includes bibliographical references.

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N2 - Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound. Objective: To elucidate the protective effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs). Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (??m) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of L-carnitine. Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.

AB - Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound. Objective: To elucidate the protective effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs). Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (??m) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of L-carnitine. Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ??m loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.

KW - Apoptosis

KW - Diabetic retinopathy

KW - Glucose

KW - L-Carnitine

KW - Oxidative stress

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