Salidroside Ameliorates Radiation Damage by Reducing Mitochondrial Oxidative Stress in the Submandibular Gland

Radiotherapy for patients with head and neck cancer inevitably causes radiation damage to salivary glands (SGs). Overproduction of reactive oxygen species (ROS) leads to mitochondrial damage and is critical in the pathophysiology of SG radiation damage. However, mitochondrial-targeted treatment is u...

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Bibliographic Details
Published in:Antioxidants 2022-07, Vol.11 (7), p.1414
Main Authors: Sun, Yue-Mei, Wang, Xin-Yue, Zhou, Xin-Ru, Zhang, Chong, Liu, Ke-Jian, Zhang, Fu-Yin, Xiang, Bin
Format: Article
Language:English
Subjects:
Adenosine triphosphate
Animal models
Antioxidants
Apoptosis
Cancer therapies
Caspase-3
Catalase
Cytochrome
Cytochrome c
Cytology
Exocrine glands
Glutathione
Head & neck cancer
Membrane potential
Mitochondria
mitochondrion
Oxidative stress
radiation damage
Radiation therapy
Reactive oxygen species
salidroside
Saliva
Salivary gland
Submandibular gland
Superoxide dismutase
Transmission electron microscopy
Ultrastructure
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Summary:Radiotherapy for patients with head and neck cancer inevitably causes radiation damage to salivary glands (SGs). Overproduction of reactive oxygen species (ROS) leads to mitochondrial damage and is critical in the pathophysiology of SG radiation damage. However, mitochondrial-targeted treatment is unavailable. Herein, both in vitro and in vivo models of radiation-damaged rat submandibular glands (SMGs) were used to investigate the potential role of salidroside in protecting irradiated SGs. Cell morphology was observed with an inverted phase-contrast microscope. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), mitochondrial ROS, mitochondrial membrane potential (MMP), and ATP were measured using relevant kits. The mitochondrial ultrastructure was observed under transmission electron microscopy. Cell apoptosis was determined by Western blot and TUNEL assays. Saliva was measured from Wharton’s duct. We found that salidroside protected SMG cells and tissues against radiation and improved the secretion function. Moreover, salidroside enhanced the antioxidant defense by decreasing MDA, increasing SOD, CAT, and GSH, and scavenging mitochondrial ROS. Furthermore, salidroside rescued the mitochondrial ultrastructure, preserved MMP and ATP, suppressed cytosolic cytochrome c and cleaved caspase 3 expression, and inhibited cell apoptosis. Together, these findings first identify salidroside as a mitochondrial-targeted antioxidant for preventing SG radiation damage.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11071414