To investigate the treatment effect and mechanism of Yangyin Shengji powder in oral ulcer after chemotherapy. The experiments were externally administered. The threshold of pain reflex (Tr) was measured 30, 60, and 120 min after the last relative substances administration to the plantar and abdomen of mice by intelligent hot plate instrument. The toe swelling degree of mice was calculated 1, 3, and 5 h after inflammation. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), and prostaglandin E2 (PGE2) were determined by enzyme-linked immunosorbent assay (ELISA), and the relative expression levels of cyclooxygenase-1 (COX-1) and COX-2 were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Two hours after the last spraying treatment, the ulcer area of mice was measured. Tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), epidermal growth factor (EGF), and epidermal growth factor receptor (EGFR) were detected by ELISA. The degree of oral mucosal injury was observed by hematoxylin and eosin (HE) staining. Compared with positive control group, the Tr value of Yangyin Shengji powder group was lower at 30 and 60 min, and the Tr value was higher at 120 min. Yangyin Shengji powder decreased the swelling degree of toes 1, 3, and 5 h after inflammation, and the SOD and GSH-Px levels in the swelling tissue of toes were significantly increased. The MDA, PGE2, COX-1 and COX-2 levels were significantly decreased. The oral mucosa structure of mice in the Yangyin Shengji powder group was relatively intact and a few inflammatory cells were infiltrated. Compared with normal group, the levels of TNF-α and IL-6 in the model group were increased, while the levels of EGF and EGFR were decreased (P<0.01). Compared with the model group, ulcer area, TNF-α, and IL-6 levels were decreased in the Yangyin Shengji powder group, while EGF and EGFR levels were increased (P<0.01). Yangyin Shengji powder has anti-inflammatory and analgesic effects, is anti-oxidative stress, inhibits inflammatory response, and inhibits the COX-2/PGE2 signaling pathway, so as to alleviate local inflammation of oral ulcer in mice after chemotherapy and promote wound healing.
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