scholarly journals Early applications of granulocyte colony-stimulating factor (G-CSF) can stabilize the blood–optic-nerve barrier and ameliorate inflammation in a rat model of anterior ischemic optic neuropathy (rAION)

2016 ◽  
Vol 9 (10) ◽  
pp. 1193-1202 ◽  
Author(s):  
Yao-Tseng Wen ◽  
Tzu-Lun Huang ◽  
Sung-Ping Huang ◽  
Chung-Hsing Chang ◽  
Rong-Kung Tsai
Keyword(s):  
Optic Nerve ◽  
Optic Neuropathy ◽  
Rat Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Factor G

scholarly journals Intravitreal Injection of Long-Acting Pegylated Granulocyte Colony-Stimulating Factor Provides Neuroprotective Effects via Antioxidant Response in a Rat Model of Traumatic Optic Neuropathy

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1934
Author(s):  
Chin-Te Huang ◽  
Yao-Tseng Wen ◽  
Tushar Dnyaneshwar Desai ◽  
Rong-Kung Tsai
Keyword(s):  
Optic Nerve ◽  
Intravitreal Injection ◽  
Optic Neuropathy ◽  
Rat Model ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Traumatic Optic Neuropathy ◽  
Neuroprotective Effects ◽  
Long Acting ◽  
Stimulating Factor

Traumatic optic neuropathy (TON) may cause severe visual loss following direct or indirect head trauma which may result in optic nerve injuries and therefore contribute to the subsequent loss of retinal ganglion cells by inflammatory mediators and reactive oxygen species (ROS). Granulocyte colony-stimulating factor (G-CSF) provides the anti-inflammatory and anti-oxidative actions but has a short half-life and also induces leukocytosis upon typical systemic administration. The purpose of the present study was to investigate the relationship between the anti-oxidative response and neuroprotective effects of long-acting pegylated human G-CSF (PEG-G-CSF) in a rat model of optic nerve crush (ONC). Adult male Wistar rats (150–180 g) were chosen to have a sham operation in one eye and have ONC in the other. PEG-G-CSF or phosphate-buffered saline (PBS control) was immediately administered after ONC by intravitreal injection (IVI). We found the IVI of PEG-G-CSF does not induce systemic leukocytosis, but increases survival of RGCs and preserves the visual function after ONC. TUNEL assays showed fewer apoptotic cells in the retina in the PEG-G-CSF-treated eyes. The number of sorely ED1-positive cells was attenuated at the lesion site in the PEG-G-CSF-treated eyes. Immunoblotting showed up-regulation of p-Akt1, Nrf2, Sirt3, and HO-1 in the ON of the PEG-G-CSF-treated eyes. Our results demonstrated that one IVI of long-acting PEG-G-CSF is neuroprotective in the rONC. PEG-G-CSF activates the p-Akt1/Nrf2/Sirt3 and the p-Akt1/Nrf2/HO-1 axes to provide the antioxidative action and further attenuated RGC apoptosis and neuroinflammation. This provides crucial preclinical information for the development of alternative therapy with IVI of PEG-G-CSF in TON.

Efficacy of Vincamine treatment in a rat model of anterior ischemic optic neuropathy

2020 ◽  
pp. 112067212097428
Author(s):  
Lu Li ◽  
Yu Su ◽  
Juejun Liu ◽  
Changzheng Chen
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Rat Model ◽  
Ganglion Cells ◽  
Nutrition Therapy ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Ischemic Tissue

Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by the progressive and irreversible death of retinal ganglion cells (RGCs) which is caused by the insufficient blood supply to the optic nerve (ON) head. At present, hormone therapy is used to reduce optic edema, followed by nerve nutrition therapy to protect the ON. However, no surgical or medical therapy has proven to be beneficial consistently in treating NAION. Vincamine is an alkaloid extracted from the Apocynaceae Vinca plant. Vincamine and its derivatives acting as cerebral vasodilators can easily cross the blood-brain barrier, improve the metabolism of ischemic tissue and protect the neuron. In this study, we aimed to investigate the potential neuroprotection of Vincamine in the photodynamic induced rat model of NAION (rAION), to evaluate its effects and possible mechanisms. We found that Vincamine can rescue RGC death and reduce the number of apoptotic cells. The protection of Vincamine might play through the PI3K/Akt/eNOS signaling pathway. Therefore, Vincamine can be an effective therapy method for NAION.

scholarly journals Can granulocyte colony stimulating factor (G-CSF) ameliorate acetaminophen-induced hepatotoxicity?

2021 ◽  
pp. 096032712110085
Author(s):  
EA Ahmed ◽  
AM Abd-Eldayem ◽  
E Ahmed
Keyword(s):  
Liver Damage ◽  
Liver Toxicity ◽  
Serum Levels ◽  
Hepatic Tissue ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Oxidative Markers ◽  
Stimulating Factor ◽  
New Strategies ◽  
Factor G

Acetaminophen (APAP) is often used as an antipyretic and analgesic agent. Overdose hepatotoxicity, which often results in liver cell failure and liver transplantation, is a severe complication of APAP usage. To save the liver and save lives from acute liver damage caused by APAP, the search for new strategies for liver defense is important. Wistar rats have been used for the induction of APAP hepatotoxicity. Elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were evaluated for liver toxicity. In addition, the levels of hepatic tissue oxidative markers such as malondialdehyde (MDA), nitric oxide (NO) increased while glutathione (GSH) was depleted and catalase (CAT) activity was curtailed. The biochemical findings were consistent with the changes in histology that suggested liver damage and inflammation. Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high. After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity. Treatment with N-AC and G-CSF after administration of APAP has also attenuated inflammation and hepatocytes necrosis. The results of this study showed that G-CSF could be viewed as an alternative hepatoprotective agent against APAP-induced acute liver injury compared to N-AC.

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