Frontiers in immunology · 2026
Effects of Batri-7 on fallopian tube tissues in a rat model of salpingitis based on the toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappa B signalling pathway.
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Yu Rong, Wu Qiutong, Xu Yanhua, Xiao Tianling, Sachurila, Li Hui, Li Genyu
Аннотация
OBJECTIVE: This study aimed to explore the underlying mechanism of Batri-7 in tubal inflammatory infertility model rats treatment in the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor kappa B (NF-κB) pathway.
METHODS: Fifty-three specific-pathogen-free-grade female Sprague-Dawley rats were selected, of which 10 were randomly assigned to the blank control group (normal rats). The remaining 43 rats were used to establish a salpingitis model, induced by mixed bacteria, and were randomly divided into a model group, a positive control group, a low-dose experimental group and a high-dose experimental group. The rats in the blank and model groups were gavaged with 10 mL·kg-1·d-1 distilled water, a Jingangteng Capsules suspension (0.4 g·kg-1) was used for the positive control group and a high-dose (0.5g·kg-1) and low-dose (0.3g·kg-1) once a day was used for the treatment groups. The rats were sacrificed after 28 days, and the fallopian tube tissue was collected after blood collection from the abdominal aorta. The contents of interleukin-1 beta (IL-1β), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1) and tumour necrosis factor-alpha (TNF-α) in plasma were detected by enzyme-linked immunosorbent assay. Protein expression was evaluated using immunohistochemistry and western blot.
RESULTS: Compared with the model group, the high-dose experimental group, the low-dose experimental group and the positive control group could significantly reduce the expression levels of IL-1β, ICAM-1 and TNF-α in plasma, increase the expression level of IL-10 (p < 0.05) and significantly reduce the expression of TLR4 and MyD88 proteins in fallopian tube tissues (p < 0.05). The improvement in each index in the high-dose experimental group was significantly better than that in the low-dose experimental group and the positive control group (p < 0.05).
CONCLUSION: Batri-7 can exert anti-inflammatory effects and treat salpingitis by regulating the TLR4/MyD8/NF-κB signalling pathway.
METHODS: Fifty-three specific-pathogen-free-grade female Sprague-Dawley rats were selected, of which 10 were randomly assigned to the blank control group (normal rats). The remaining 43 rats were used to establish a salpingitis model, induced by mixed bacteria, and were randomly divided into a model group, a positive control group, a low-dose experimental group and a high-dose experimental group. The rats in the blank and model groups were gavaged with 10 mL·kg-1·d-1 distilled water, a Jingangteng Capsules suspension (0.4 g·kg-1) was used for the positive control group and a high-dose (0.5g·kg-1) and low-dose (0.3g·kg-1) once a day was used for the treatment groups. The rats were sacrificed after 28 days, and the fallopian tube tissue was collected after blood collection from the abdominal aorta. The contents of interleukin-1 beta (IL-1β), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1) and tumour necrosis factor-alpha (TNF-α) in plasma were detected by enzyme-linked immunosorbent assay. Protein expression was evaluated using immunohistochemistry and western blot.
RESULTS: Compared with the model group, the high-dose experimental group, the low-dose experimental group and the positive control group could significantly reduce the expression levels of IL-1β, ICAM-1 and TNF-α in plasma, increase the expression level of IL-10 (p < 0.05) and significantly reduce the expression of TLR4 and MyD88 proteins in fallopian tube tissues (p < 0.05). The improvement in each index in the high-dose experimental group was significantly better than that in the low-dose experimental group and the positive control group (p < 0.05).
CONCLUSION: Batri-7 can exert anti-inflammatory effects and treat salpingitis by regulating the TLR4/MyD8/NF-κB signalling pathway.