Lin Jian,Li Xican,Han Lu,Li Fei,Lu Wenbiao,Bai Ye,Chen Dongfeng
Background In the study, Folium Sennae (FS) was firstly extracted by various solvents to obtain five FS extracts. Then, five FS extracts were evaluated for the protective effects against •OH-induced DNA damage, antioxidant abilities in vitro, and chemical contents using various methods. On this basis, the correlation graphs between the pharmacological effects and chemical contents were plotted to obtain the correlation coefficients (R values). Finally, in order to obtain biological evidence, ethyl acetate extract of FS (EAFS) was investigated for the protective effect against •OH-induced MSCs (mesenchymal stem cells) damage using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl) assay. Results The pharmacological assays indicated that five FS extracts could effectively protect against •OH-induced DNA damage. The correlation analysis suggested that the average R values of total phenolics, total anthraquinones, aloe-emodin, rhein, and emodin were respectively 0.843, 0.833, 0.753, 0.820, and 0.784, while those of total sugars and total saponins were respectively 0.103 and 0.0068. The mechanistic analysis revealed that five FS extracts could also scavenge •OH, •O 2 – , DPPH• & ABTS• + radicals, and reduce Cu 2+ to Cu + . MTT assay revealed that the viability of MSCs which were treated with •OH radicals has been effectively protected by EAFS (3 and 30 μg/mL). Conclusion On this basis, it can be concluded that: ( i ) Folium Sennae exhibits a protective effect against •OH-induced damages to DNA and MSCs; ( ii ) The effects may be attributed to phytophenols (especially aloe-emodin, rhein, and emodin), not sugars or saponins; ( iii ) They exert the protective action via hydrogen atom transfer (HAT) and/or sequential electron proton transfer (SEPT) mechanisms which make phenolic –OH moiety be oxidized to stable semi-quinone form; ( iv ) The stability of semi-quinone form can ultimately be responsible for the protective or antioxidant effect of phytophenols.
Chunlian Liu,Chengcheng Song,Yan Wang,Yangxin Xiao,Zhongshi Zhou,Guosheng Cao,Xiongjie Sun,Yanju Liu
Ethnopharmacological relevance Atractylodes lancea (Thunb.) DC. is a Chinese herb that has been commonly used to treat spleen-deficiency diarrhea (SDD) in China for over a thousand years. However, the underlying mechanism of its antidiarrheal activity is not fully understood. Aim of the study The antidiarrheal effects of the ethanol extract of deep-fried A. lancea rhizome (EEDAR) due to spleen deficiency induced by folium sennae (SE) were determined on the regulation of the short-chain fatty acid (SCFA) metabonomics induced by the intestinal flora . Materials and methods The effects of EEDAR on a SE-induced mouse model of SDD were evaluated by monitoring the animal weight, fecal water content, diarrhea-grade rating, goblet cell loss, and pathological changes in the colon. The expression of inflammatory factors (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, IL-6, IL-10), aquaporins (AQP3, AQP4, and AQP8), and tight junction markers (ZO-1, occludin , claudin-1) in colon tissues were determined using quantitative polymerase chain reaction and western blotting . SCFA metabonomics in the feces of mice treated with EEDAR was evaluated using gas chromatography–mass spectrometry. Furthermore, 16S rDNA sequencing was used to determine the effect of EEDAR on the intestinal flora of SDD mice, and fecal microbiota transplantation (FMT) was used to confirm whether the intestinal flora was essential for the anti-SDD effect of EEDAR. Results Treatment with EEDAR significantly improved the symptoms of mice with SDD by inhibiting the loss of colonic cup cells, alleviating colitis , and promoting the expression of AQPs and tight junction markers. More importantly, the effect of EEDAR on the increase of SCFA content in mice with SDD was closely related to the gut microbiota composition. EEDAR intervention did not significantly improve intestinal inflammation or the barrier of germ-free SDD mice, but FMT was effective. Conclusion EEDAR alleviated SE-induced SDD in mice, as well as the induced SCFA disorder by regulating the imbalance of the intestinal microbiota.
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