Effect of enhanced aryl hydrocarbon receptor expression on inflammatory response and healing of alveolar bone defects in diabetic rats

doi:10.3969/j.issn.2095-4344.3144

Abstract

Abstract: BACKGROUND: Under high glucose conditions, inflammatory responses in the defect site of alveolar bone are intensified, resulting in delayed bone healing. Previous studies have shown that enhanced aryl hydrocarbon receptor (AhR) expression can inhibit inflammatory responses and promote tissue healing.
OBJECTIVE: To study the effect and mechanism of enhanced AhR expression on inflammatory response and healing of alveolar bone defects in diabetic rats.
METHODS: Ten of 40 Sprague-Dawley rats were randomly selected as normal controls. Diabetic models were established in the other 30 rats, and randomly divided into AhR enhancement, negative control, and blank control groups, with 10 rats in each group. Bone defects were made by surgery in both sides of maxillae of each diabetic rat. After surgery, AteloGene gel with AhR lentiviruses was injected into the defect sites of rats in the AhR enhancement group. AteloGene gel with control lentiviruses was injected into the defect sites of rats in the negative control group. Rats in blank control group and normal control group received no injection. Twenty-eight days after defects were made, all rats were sacrificed, and left maxillary bone tissues were collected to detect bone healing using hematoxylin-eosin staining. Tissues from right maxillary bone defect sites were detached, and qRT-PCR was used to detect the gene expression of AhR and Notch signaling pathway members and inflammatory factors and alkaline phosphatase. Animal experiment was approved by the Animal Experimental Ethics Committee of Guangxi Medical University.
RESULTS AND CONCLUSION: Hematoxylin-eosin staining showed that the Lane-Sandhu scores of bone tissue regeneration in the AhR enhancement group were higher than those of negative control and blank control groups (P < 0.05); and the levels of inflammatory cell infiltration were lower than those of negative control and blank control groups (P < 0.05). qRT-PCR results showed that the levels of tumor necrosis factor α, interleukin-6, Notch1, Jagged1 levels, and Jagged2 in the AhR enhancement group were lower than those in the negative control and blank control groups (P < 0.05), and the levels of interleukin-10 and alkaline phosphatase were higher than those in the negative control and blank control groups (P < 0.05). These findings suggest that under high glucose conditions, enhanced AhR expression could reduce inflammatory response in alveolar bone defect sites of diabetic rats and promote the healing of bone defects, which may be associated with the inhibition of Notch signaling activation.

Key words: diabetes mellitus, alveolar bone defect, inflammatory response, receptor, bone defect, signaling pathway, inflammatory response, alkaline phosphatase, rat

CLC Number:

Luo Yicai, Li Hao. Effect of enhanced aryl hydrocarbon receptor expression on inflammatory response and healing of alveolar bone defects in diabetic rats[J]. Chinese Journal of Tissue Engineering Research, 2021, 25(14): 2166-2171.

Figures/Tables 4

References

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