Clinical and experimental gastroenterology · 2026
Assessment of the Biological Effect of Oral Ginkgolic Acid Liposome Nanoparticles for Treating Refractory Helicobacter pylori Infection.
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Xu Jingwen, Zhang Chengbo, Jiang Yan, Wang Rumeng, Liu Yang, Zhang Ning, Liu Yugang, Jia Lizhou
Аннотация
OBJECTIVE: To explore the antibacterial effect of ginkgolic acid (GA) modified into liposome nanoparticles (TLM@GA) against Helicobacter pylori and investigate the antibacterial mechanism involved to provide a lead drug for radical clinical treatment.
METHODS: A new complex that improved GA stability and bioavailability was constructed using liposome nanoparticles (TLM@GA). The construction of the complex was verified by Fourier transform infrared spectroscopy, scanning electron microscopy, Zeta potential, and particle size detection, and its physicochemical properties were comprehensively evaluated. An acute gastritis model was also established using C57BL/6 mice, in which the in vivo therapeutic effect of TLM@GA was evaluated by detecting the colonization amount of the clinical multi-resistant strain HPBS001 in the gastric mucosa. Additionally, the pathological inflammation of the gastric mucosa was observed with H&E staining, apoptosis of gastric mucosal cells was observed with TUNEL staining, and the expression of serum inflammatory factors was detected with enzyme-linked immunosorbent assay. The in vivo safety of TLM@GA was evaluated by detecting its effect on mouse body weight and the damage to the stomach, liver, spleen, and kidneys.
RESULTS: The TLM@GA complex had excellent stability and dispersibility. The minimum inhibitory concentration of GA against H. pylori strains was 16-32 μg/mL, and that of TLM@GA was 0.25-0.5 μg/mL. After GA was modified into TLM@GA, its antibacterial activity was 32-128 times higher. After treatment with TLM@GA (28 mg/kg), the colonization of H. pylori in the gastric mucosa was significantly reduced, which was better than that in the omeprazole and amoxicillin (dual-therapy) and GA groups. Apoptotic and inflammatory cells in the gastric mucosa were significantly reduced, indicating alleviated inflammation. After treatment, the expression levels of major inflammatory factors were significantly decreased. There was no significant change in body weight when mice were intragastrically administered 140 mg/kg TLM@GA for 1 week, and no obvious pathological damage was found in the stomach, liver, spleen, or kidneys.
CONCLUSION: TLM@GA had excellent stability, efficient release, and good loading capacity efficiency. It was significantly superior to GA in terms of in vitro antibacterial activity, had low toxicity, was not prone to drug resistance, and demonstrated high safety. TLM@GA demonstrated a good antibacterial effect in the in vivo acidic environment, effectively slowing the apoptosis of gastric mucosal cells and significantly reducing levels of inflammatory factors, alleviating the inflammatory response.
METHODS: A new complex that improved GA stability and bioavailability was constructed using liposome nanoparticles (TLM@GA). The construction of the complex was verified by Fourier transform infrared spectroscopy, scanning electron microscopy, Zeta potential, and particle size detection, and its physicochemical properties were comprehensively evaluated. An acute gastritis model was also established using C57BL/6 mice, in which the in vivo therapeutic effect of TLM@GA was evaluated by detecting the colonization amount of the clinical multi-resistant strain HPBS001 in the gastric mucosa. Additionally, the pathological inflammation of the gastric mucosa was observed with H&E staining, apoptosis of gastric mucosal cells was observed with TUNEL staining, and the expression of serum inflammatory factors was detected with enzyme-linked immunosorbent assay. The in vivo safety of TLM@GA was evaluated by detecting its effect on mouse body weight and the damage to the stomach, liver, spleen, and kidneys.
RESULTS: The TLM@GA complex had excellent stability and dispersibility. The minimum inhibitory concentration of GA against H. pylori strains was 16-32 μg/mL, and that of TLM@GA was 0.25-0.5 μg/mL. After GA was modified into TLM@GA, its antibacterial activity was 32-128 times higher. After treatment with TLM@GA (28 mg/kg), the colonization of H. pylori in the gastric mucosa was significantly reduced, which was better than that in the omeprazole and amoxicillin (dual-therapy) and GA groups. Apoptotic and inflammatory cells in the gastric mucosa were significantly reduced, indicating alleviated inflammation. After treatment, the expression levels of major inflammatory factors were significantly decreased. There was no significant change in body weight when mice were intragastrically administered 140 mg/kg TLM@GA for 1 week, and no obvious pathological damage was found in the stomach, liver, spleen, or kidneys.
CONCLUSION: TLM@GA had excellent stability, efficient release, and good loading capacity efficiency. It was significantly superior to GA in terms of in vitro antibacterial activity, had low toxicity, was not prone to drug resistance, and demonstrated high safety. TLM@GA demonstrated a good antibacterial effect in the in vivo acidic environment, effectively slowing the apoptosis of gastric mucosal cells and significantly reducing levels of inflammatory factors, alleviating the inflammatory response.