Mechanism of Thunder-Fire Moxibustion in the Treatment of Meibomian Gland Dysfunction Induced by High-Fat Diet.

Objective: An investigation into whether Thunder-Fire Moxibustion improves Meibomian Gland Dysfunction by activating peroxisome proliferator-activated receptor gamma (PPARγ)-related signaling pathway.

Methods: C57BL/6 mice were randomly divided into a Control Group (CG), model group (MG), Experimental Group (EG), Treatment Group (TG), and GW9662 (GW), with 10 mice in each group. The obstruction of the meibomian gland opening, tear film rupture time, and corneal fluorescein sodium staining were observed. The morphology of the meibomian gland was observed by HE staining. Observations of oil red staining were made on the meibomian gland to determine its oil content. The expression levels of PPARγ, NF-κB p65, Phospho-NF-κB p65 (p-NF-κB), and IL-6 in the meibomian gland were detected by Western blot. The expression of PPARγ, NF-κB p65, p-NF-κB p65, and IL-6 in the meibomian gland was examined by immunofluorescence staining.

Results: The results showed that compared to the Control Group, the Model Group mice exhibited an increased Meibomian Gland Orifices Score (MGOS) (P < .01), an increased MG corneal staining (P < .01), a shorter tear film break-up time (P < .01), eyelid atrophy, disordered arrangement of meibomian gland cells, the presence of a large number of immature adipocytes, varying degrees of cellular inflammation and infiltration, a significant reduction in meibomian gland tissue lipids, decreased expressions of MGPPARγ and NF-κB (P < .01), and elevated expressions of phosphorylated NF-κB and IL-6 (P < .01). However, Western medicine, antagonists, and thunder-fire moxibustion were all able to reverse these phenomena observed in the Model Group mice (P < .01), with thunder-fire moxibustion exhibiting the most significant effect (P < .01).

Conclusion: The thunder-fire moxibustion can induce the differentiation of meibomian gland cells, thereby improving the inflammation response.