Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Ali Serdar Oğuzoğlu; Halil Aşçı; Musa Canan; Nilgün Şenol; Özlem Özmen

Article Details

Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Authors:

Ali Serdar Oğuzoğlu | Halil Aşçı | Musa Canan | Nilgün Şenol | Özlem Özmen

Publisher:

Süleyman Demirel University

Main Topics:

Brain and Nerve Surgery (Neurosurgery)

Journal:

Medical Journal of Süleyman Demirel University Vol.31 Issue 4, pp.310-317

Document Type:

Article

Publication Date:

12/2024

Document Language:

English

Document ID (Org No.):

2001335525

pISSN:

1300-7416

Keywords:

Abstract:

 Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage SAH can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10 formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor BDNF and neurofilament NF in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase Cas-3, hypoxia-inducible factor 1 alpha Hif-1α and nuclear factor kappa beta NF-κB expressions in the lung, Cas-5, cyclooxygenase-1 Cox-1 and interleukin IL-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

 Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage SAH can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10 formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor BDNF and neurofilament NF in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase Cas-3, hypoxia-inducible factor 1 alpha Hif-1α and nuclear factor kappa beta NF-κB expressions in the lung, Cas-5, cyclooxygenase-1 Cox-1 and interleukin IL-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

 Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage SAH can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10 formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor BDNF and neurofilament NF in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase Cas-3, hypoxia-inducible factor 1 alpha Hif-1α and nuclear factor kappa beta NF-κB expressions in the lung, Cas-5, cyclooxygenase-1 Cox-1 and interleukin IL-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

 Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage SAH can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10 formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor BDNF and neurofilament NF in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase Cas-3, hypoxia-inducible factor 1 alpha Hif-1α and nuclear factor kappa beta NF-κB expressions in the lung, Cas-5, cyclooxygenase-1 Cox-1 and interleukin IL-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

Article Details

Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Authors:

Ali Serdar Oğuzoğlu | Halil Aşçı | Musa Canan | Nilgün Şenol | Özlem Özmen

Publisher:

Süleyman Demirel University

Main Topics:

Brain and Nerve Surgery (Neurosurgery)

Journal:

Medical Journal of Süleyman Demirel University Vol.31 Issue 4, pp.310-317

Document Type:

Article

Publication Date:

12/2024

Document Language:

English

Document ID (Org No.):

2001335525

pISSN:

1300-7416

Subarachnoid hemorrhage

Liver

Lung

Kidney

inflammation

apoptosis

Issues

Article Details

Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Authors: Ali Serdar Oğuzoğlu | Halil Aşçı | Musa Canan | Nilgün Şenol | Özlem Özmen

Publisher: Süleyman Demirel University

Main Topics: Brain and Nerve Surgery (Neurosurgery)

Journal: Medical Journal of Süleyman Demirel University Vol.31 Issue 4, pp.310-317

Document Type: Article

Publication Date: 12/2024

Document Language: English

Document ID (Org No.): 2001335525

pISSN: 1300-7416

Subarachnoid hemorrhage

Liver

Lung

Kidney

inflammation

apoptosis

Issues

Authors:

Ali Serdar Oğuzoğlu | Halil Aşçı | Musa Canan | Nilgün Şenol | Özlem Özmen

Publisher:

Süleyman Demirel University

Main Topics:

Brain and Nerve Surgery (Neurosurgery)

Journal:

Medical Journal of Süleyman Demirel University Vol.31 Issue 4, pp.310-317

Document Type:

Article

Publication Date:

12/2024

Document Language:

English

Document ID (Org No.):

2001335525

pISSN:

1300-7416