Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Rosa chinensis cv. 'JinBian' flowers alleviates brain damage and cognitive deficit by inhibiting ferroptosis via the Keap1/Nrf2/GPX4 pathway and regulating gut microbiota.
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Zhen Li, Peng Jianhong, Cui Huimin, Tao Junhong, Liu Yaping, Cao Jianxin, El-Seedi Hesham R, Cheng Guiguang, Wang Zhengxuan
Аннотация
BACKGROUND: The flowers of Rosa chinensis cv. 'JinBian' (RCF) has been utilized as a herbal tea for millennia to prevent aging-related diseases. RCF is enriched in flavonoids and exhibits significant antioxidant effects for anti-aging potential. However, the specific bioactive compounds and their underlying anti-aging mechanisms remain unclear.
PURPOSE: This study aimed to investigate the bioactive ingredients and neuroprotective mechanisms of RCF extracts.
METHODS: The study obtained dichloromethane (RD), ethyl acetate (RE), n-butanol (RB), and residual water (RW) fractions from RCF after liquid-liquid extraction. It investigated their neuroprotective effect in in vitro and in vivo experiments. UHPLC-ESI-HRMS/MS analysis was used to identify phytochemicals in RE. In vitro assays included measuring phenolic and flavonoid contents, ABTS⁺ and DPPH+ scavenging capacities, and effects on H₂O₂-induced SHSY-5Y cells. In vivo, D-galactose-induced mice were used and assessed through the Morris water maze test and the crucifixion anxiety test. Molecular pathways and gut microbiota were analyzed.
RESULTS: Among the fractions, RE had the highest phenolic and flavonoid contents, the strongest ABTS⁺ and DPPH+ scavenging capacities, and significantly inhibited ROS accumulation by increasing the antioxidant ability (GSH, CAT, SOD) in H₂O₂-induced SHSY-5Y cells. UHPLC-ESI-HRMS/MS analysis identified 28 phytochemicals in RE, primarily gallic acid derivatives and flavonoid derivatives. In D-galactose-induced mice, RE alleviated memory impairment and anxiety-like behavior. RE ameliorated brain damage by activating the Keap1/Nrf2-regulated antioxidant pathway (increasing T-AOC, GSH, GPX4, NQO1, SOD1, HO-1), suppressing ferroptosis, inhibiting acetylcholinesterase activity, attenuating GSK-3β/Tau/Bcl-2 axis-regulated apoptosis, and modulating AMPK-regulated autophagy. Additionally, RE improved gut microbiota diversity, particularly increasing beneficial bacteria such as Lactobacillus and Bifidobacterium.
CONCLUSIONS: Therefore, RE could alleviate the cognitive deficit associated with age-related neurodegenerative diseases by targeting ferroptosis-related oxidative stress, apoptosis, and autophagy, as well as modulating the gut microbiota.
PURPOSE: This study aimed to investigate the bioactive ingredients and neuroprotective mechanisms of RCF extracts.
METHODS: The study obtained dichloromethane (RD), ethyl acetate (RE), n-butanol (RB), and residual water (RW) fractions from RCF after liquid-liquid extraction. It investigated their neuroprotective effect in in vitro and in vivo experiments. UHPLC-ESI-HRMS/MS analysis was used to identify phytochemicals in RE. In vitro assays included measuring phenolic and flavonoid contents, ABTS⁺ and DPPH+ scavenging capacities, and effects on H₂O₂-induced SHSY-5Y cells. In vivo, D-galactose-induced mice were used and assessed through the Morris water maze test and the crucifixion anxiety test. Molecular pathways and gut microbiota were analyzed.
RESULTS: Among the fractions, RE had the highest phenolic and flavonoid contents, the strongest ABTS⁺ and DPPH+ scavenging capacities, and significantly inhibited ROS accumulation by increasing the antioxidant ability (GSH, CAT, SOD) in H₂O₂-induced SHSY-5Y cells. UHPLC-ESI-HRMS/MS analysis identified 28 phytochemicals in RE, primarily gallic acid derivatives and flavonoid derivatives. In D-galactose-induced mice, RE alleviated memory impairment and anxiety-like behavior. RE ameliorated brain damage by activating the Keap1/Nrf2-regulated antioxidant pathway (increasing T-AOC, GSH, GPX4, NQO1, SOD1, HO-1), suppressing ferroptosis, inhibiting acetylcholinesterase activity, attenuating GSK-3β/Tau/Bcl-2 axis-regulated apoptosis, and modulating AMPK-regulated autophagy. Additionally, RE improved gut microbiota diversity, particularly increasing beneficial bacteria such as Lactobacillus and Bifidobacterium.
CONCLUSIONS: Therefore, RE could alleviate the cognitive deficit associated with age-related neurodegenerative diseases by targeting ferroptosis-related oxidative stress, apoptosis, and autophagy, as well as modulating the gut microbiota.