The administration of oral mucosal mesenchymal-derived stem cells improves hepatic inflammation, oxidative stress, and histopathology following traumatic brain injury

被引:0
|
作者
Alizadeh, Eshagh [1 ,2 ]
Sabet, Nazanin [3 ]
Soltani, Zahra [4 ,5 ]
Khaksari, Mohammad [4 ,5 ]
Jafari, Elham [6 ]
Karamouzian, Saeed [1 ,2 ]
机构
[1] Kerman Univ Med Sci, Inst Basic & Clin Physiol Sci, Cardiovasc Res Ctr, Kerman, Iran
[2] Kerman Univ Med Sci, Dept Neurosurg, Kerman, Iran
[3] Kerman Univ Med Sci, Inst Neuropharmacol, Physiol Res Ctr, Kerman, Iran
[4] Kerman Univ Med Sci, Inst Basic & Clin Physiol Sci, Fac Med, Endocrinol & Metab Res Ctr, Kerman, Iran
[5] Kerman Univ Med Sci, Afzalipour Fac Med, Dept Physiol & Pharmacol, Kerman, Iran
[6] Kerman Univ Med Sci, Pathol & Stem Cells Res Ctr, Sch Med, Dept Pathol, Kerman, Iran
关键词
Traumatic brain injury; Stem cells; Inflammation; Oxidative stress; Liver; INDUCED LIVER-INJURY; RAT; STAT3; PROGESTERONE; EPIDEMIOLOGY; ANTIOXIDANT; INVOLVEMENT;
D O I
10.1016/j.trim.2023.101950
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: The inflammatory mediators produced after traumatic brain injury (TBI) are reaching peripheral organs causing organ and tissue damage, including the liver. Our study assessed the effect of intravenous (i.v.) infusion of oral mesenchymal stem cells (OMSCs) on TBI-induced liver damage by measuring liver inflammatory factors and liver oxidative stress. Methods: Twenty-eight adult male Wistar rats were divided into four groups: 1) sham control; 2) TBI alone (TBI); 3) TBI vehicle (Veh)-control; and 4) TBI with OMSC treatment (SC). OMSCs were obtained from oral mucosa biopsies. OMSCs were administered and administered i.v. at 1 and 24 h after TBI. Within 48 h after TBI, multiple parameters were analyzed, including inflammation, oxidative stress, and histopathological changes. Results: In comparison to sham controls, the TBI alone showed in liver significantly increased levels of interleukin-1 beta (IL-1 beta; P < 0.001), interleukin-6 (IL-6; P < 0.001), malondialdehyde (MDA; P < 0.001), and protein carbonyl (PC; P < 0.001). At the same time the TBI alone decreased the liver levels of superoxide dismutase (SOD; P < 0.001), total antioxidant capacity (TAC; P < 0.001), catalase (CAT; P < 0.001), and interleukin-10 (IL10; P < 0.001). In comparison to the TBI alone group, the therapeutic group treated with i.v. infusion of OMSCs demonstrated significantly reduced changes of IL-1 beta (P < 0.001), IL-6 (P < 0.01), MDA (P < 0.01), PC (P < 0.05), SOD (P < 0.001), TAC (P < 0.01), CAT (P < 0.01), and IL-10 (P < 0.01). Histopathological evaluation showed in TBI alone group that the total score of liver tissue injury included extensive hydropic degeneration, lobular necrosis, inflammation as well as central vein congestion with subendothelial hemorrhage increased compared the sham group (P < 0.001). Administration of OMSC showed significantly smaller increase in the injury score compared to the TBI alone group (P < 0.001). Conclusion: Therapy with i.v. OMSCs administration after TBI reduces liver injury, as measured by inflammation and oxidative stress. The use of OMSCs can be considered for treatment of liver injury caused by TBI.
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页数:8
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