International immunopharmacology · 2025
Panax notoginseng protects blood-retinal barrier by modulating microglia polarization via TLR4/MyD88/NF-κB pathway in endotoxin-induced uveitis.
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Peng Meizhong, Ning Shangqiu, Wu Yan, Yang Meimei, Zhang Yifei, Hu Tengyue, Yuan Yueying, Zhang Yuting, Hao Gaimei, Han Jing
Аннотация
BACKGROUND: Panax notoginseng is a traditional Chinese medicine for promoting blood circulation and removing blood stasis. Panax notoginseng compound is widely used in the treatment of uveitis, however, the current research focuses on the compound, and the role of Panax notoginseng in the compound has not been elucidated.
OBJECTIVE: The aim of this study was to explore the effects and potential molecular mechanism of Panax notoginseng against uveitis.
METHODS: Establishment of endotoxin-induced uveitis (EIU) model in mice was induced by intravitreal injection of lipopolysaccharide, the mice were orally administrated with saline or Panax notoginseng for seven days before injection. The animals were examined for ocular inflammation using slit-lamp photography and HE staining. The biomarkers for microglia polarization and blood-retinal barrier (BRB) disruption were evaluated in the mouse retinas and BV2 cells. Western blot was used to detect the molecular mechanism of Panax notoginseng and its main active ingredients against EIU.
RESULTS: Panax notoginseng treatment significantly alleviated intraocular inflammation and increased M1 microglia to M2 microglia polarization. In addition, the dysfunction of BRB was attenuated by Panax notoginseng intervention. Panax notoginseng and its main components ginsenoside Rd, ginsenoside Rg1 and notoginsenoside R1 treatment down-regulated the expression of TLR4, MyD88 and NF-κB phosphorylation proteins in retinal tissues and BV2 cells.
CONCLUSIONS: Panax notoginseng potentially modulates M1/M2 microglia polarization by inhibiting TLR4/MyD88/NF-κB pathway, thereby maintaining BRB integrity to ameliorate EIU, more importantly, the combined intervention of ginsenoside Rd, ginsenoside Rg1 and notoginsenoside R1 exerts a similar protective effect with Panax notoginseng.
OBJECTIVE: The aim of this study was to explore the effects and potential molecular mechanism of Panax notoginseng against uveitis.
METHODS: Establishment of endotoxin-induced uveitis (EIU) model in mice was induced by intravitreal injection of lipopolysaccharide, the mice were orally administrated with saline or Panax notoginseng for seven days before injection. The animals were examined for ocular inflammation using slit-lamp photography and HE staining. The biomarkers for microglia polarization and blood-retinal barrier (BRB) disruption were evaluated in the mouse retinas and BV2 cells. Western blot was used to detect the molecular mechanism of Panax notoginseng and its main active ingredients against EIU.
RESULTS: Panax notoginseng treatment significantly alleviated intraocular inflammation and increased M1 microglia to M2 microglia polarization. In addition, the dysfunction of BRB was attenuated by Panax notoginseng intervention. Panax notoginseng and its main components ginsenoside Rd, ginsenoside Rg1 and notoginsenoside R1 treatment down-regulated the expression of TLR4, MyD88 and NF-κB phosphorylation proteins in retinal tissues and BV2 cells.
CONCLUSIONS: Panax notoginseng potentially modulates M1/M2 microglia polarization by inhibiting TLR4/MyD88/NF-κB pathway, thereby maintaining BRB integrity to ameliorate EIU, more importantly, the combined intervention of ginsenoside Rd, ginsenoside Rg1 and notoginsenoside R1 exerts a similar protective effect with Panax notoginseng.