To investigate the regulatory mechanism of Lactobacillus acidophilus ATCC 4356 on the nuclear factor kappa-B (NF-κB) signaling pathway in mice with radiation-induced oral mucositis, as well as its anti-inflammatory effect.

The experiment established a radiation-induced oral mucositis model in mice by irradiating their head and neck with X-rays. The levels of oxidative stress-related biochemical indicators and inflammatory-related cytokines in the mice’s serum were measured using kits. Subsequently, the messenger RNA(mRNA) and protein expressions in the mice’s oral tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot methods.

Lactobacillus acidophilus ATCC 4356 reduced the oral mucositis score in mice with radiation-induced oral mucositis. Lactobacillus acidophilus ATCC 4356 also increased the levels of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) in the serum of mice with radiation-induced oral mucositis and reduced the levels of NF-κB, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and malondialdehyde (MDA). Further experiments showed that Lactobacillus acidophilus ATCC 4356 could up-regulate the mRNA expression of SOD1 (Cu/Zn-SOD), CAT, glutathione peroxidase 1 (Gpx1) and inhibitor of kappa B alpha (IκBα) in the oral tissues of mice with radiation-induced oral mucositis and down-regulate the mRNA expression of heme oxygenase 1 (Hmox1), NF-κB subunit p65 (NF-κB p65), toll-like receptor 4 (TLR4) and NF-κB1 (NF-κB p50/p105). At the same time, Lactobacillus acidophilus ATCC 4356 also down-regulated the protein expression of NF-κB p65 in the oral tissues of mice with radiation-induced oral mucositis and up-regulated the protein expression of IκBα.

The experimental results confirmes that Lactobacillus acidophilus ATCC 4356 has the effect of alleviating radiation-induced oral mucositis under laboratory conditions, and it is closely related to its regulation of the NF-κB signaling pathway.