Jatrorrhizine attenuates inflammatory response in Helicobacter pylori-induced gastritis by suppressing NLRP3 inflammasomes and NF-κB signaling pathway

Helicobacter pylori (H. pylori) was demonstrated to induce gastric mucosa inflammation in chronic atrophic gastritis (CAG). Jatrorrhizine possesses numerous biological properties, including Antibacterial and anti-inflammatory effects. The present study was aimed at investigating whether Jatrorrhizine inhibits H. pylori-induced CAG and elucidating the underlying potential mechanisms. The rats were orally inoculated with H. pylori to establish CAG model. Fourteen days after Jatrorrhizine treatment, we measured the rat's body weight as well as rat's food intake. Besides, alcian blue and periodic acid-Schiff (AB-PAS) staining and hematoxylin-eosin (HE) staining were performed to observe the hisological changes of gastric mucosa. The inflammatory cytokines and gastric mucosa factors were measured by ELISA. The protein level in gastric mucosa was detected by Western blotting. H. pylori inoculation significantly induced gastric dysfunction, inflammatory infiltration and gastric mucosa injury, suggesting CAG rat model was successfully constructed. Nonetheless, Jatrorrhizine treatment effectively improved gastric function and pathological injury. Besides, Jatrorrhizine suppressed the inflammation and colonization of H. pylori in CAG rats. Moreover, Jatrorrhizine administration not only decreased inflammatory cytokines but also increased gastric mucosa factors, implying its protective effect on gastric mucosal. Mechanistically, Jatrorrhizine restrained the activation of NLRP3 inflammasomes and NF-κB signaling. Jatrorrhizine had inhibitory effects on H. pylori-induced inflammation, thus suppressing the progression of CAG via inactivation of NF-κB/NLRP3 signaling. Our findings underscore the potential of Jatrorrhizine as a promising candidate for clinical trials for CAF treatment.

Chronic atrophic gastritis; Helicobacter pylori; Jatrorrhizine; NF-κB/NLRP3.