scholarly journals (2813) Proposal to conserve the name Hedyotis diffusa ( Oldenlandia diffusa , Scleromitrion diffusum ) ( Rubiaceae ) with a conserved type

Taxon ◽  
2021 ◽  
Vol 70 (2) ◽  
pp. 443-444
Author(s):  
Tin Yan Siu ◽  
Mavis Hong Yu Yik ◽  
David E. Boufford ◽  
Pang Chui Shaw ◽  
David Tai Wai Lau
2010 ◽  
Vol 30 (3) ◽  
pp. 292-296 ◽  
Author(s):  
Wei-cheng CHEN ◽  
Da-wei GU ◽  
Hai ZHANG ◽  
Zhen-yu ZHU ◽  
Guo-qing ZHANG ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 878
Author(s):  
Ling Zhao ◽  
Jiang Deng ◽  
Zi-Jian Xu ◽  
Wan-Po Zhang ◽  
Mahmoud Mohamed Khalil ◽  
...  

The objective of this study was to explore the mechanism of Hedyotis diffusa (HD) in mediating the detoxification of aflatoxin B1 (AFB1)-induced hepatic injury in chicks. A total of 144 one-day-old male broilers (Cobb 500) were randomly assigned to four treatment groups (n = 6 cages/diet, 6 chicks/cage). After three days of acclimation, the broilers were fed either a control diet (Control), Control plus 0.5 mg/kg of AFB1, or Control plus 0.5 mg/kg AFB1 with 500 or 1000 mg/kg HD for two weeks. Both serum and liver were collected at the end of the feeding trial for biochemistry, histology, and NF-E2-related nuclear factor 2 (NRF2)/antioxidant response element (ARE) signaling analysis. Compared with Control, the AFB1 treatment caused liver injury and decreased (p < 0.05) body weight gain, feed intake, feed conversion ratio, and serum albumin and total protein by 6.2–20.7%. AFB1 also induced swelling, necrosis, and severe vacuolar degeneration in chicks’ livers. Notably, HD supplementation at 500 and 1000 mg/kg mitigated (p < 0.05) the alterations induced by AFB1. HD supplementation alleviated (p < 0.05) AFB1-induced impairment in hepatic glutathione peroxidase activity, protein carbonyl, and exo-AFB1-8,9-epoxide (AFBO)–DNA concentrations by 57.7–100% and increased (p < 0.05) the activities of superoxide dismutase and catalase by 23.1–40.9% more than those of AFB1 treatment alone. Furthermore, HD supplementation at the two doses upregulated (p < 0.05) NRF2, NAD(P)H: quinone oxidoreductase-1, heme oxygenase-1, glutathione cysteine ligase catalytic subunit, and glutathione-S transferase A2 and A3 in livers relative to the AFB1 group by 0.99–3.4-fold. Overall, dietary supplementation of HD at a high dose displayed better protection effects against aflatoxicosis. In conclusion, a dietary HD supplementation at 500 and 1000 mg/kg protected broilers from AFB1-induced hepatotoxicity, potentially due to the activation of NRF2/ARE signaling in the chicks.


2016 ◽  
pp. 255 ◽  
Author(s):  
Zengwu Shao ◽  
Feifei Pu ◽  
Fengxia Chen ◽  
Songfeng Chen ◽  
Zhicai Zhang ◽  
...  

2019 ◽  
Vol 109 ◽  
pp. 969-984 ◽  
Author(s):  
Xing Su ◽  
Yueping Li ◽  
Meng Jiang ◽  
Jinglin Zhu ◽  
Chunli Zheng ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Ya-Xin Lv ◽  
Hao-Ran Pan ◽  
Xin-Ying Song ◽  
Qing-Qi Chang ◽  
Dan-Dan Zhang

Hedyotis diffusa (HD) plus Scutellaria barbata (SB) have been widely used in antitumor clinical prescribes as one of herb pairs in China. We investigated the effect of aqueous extract from Hedyotis diffusa plus Scutellaria barbata at the equal weight ratio (HDSB11) in inhibiting the growth of murine non-small-cell lung cancer cell (NSCLC) line LLC in vivo and in vitro in this study. Compared with other aqueous extracts, HDSB11 showed the lowest IC50 in inhibiting cell proliferation at 0.43 mg/ml. Besides, HDSB11 effectively suppressed colony formation and induced cell apoptosis. The further assessment of HDSB11 on the murine Lewis-lung-carcinoma-bearing mouse model showed it significantly inhibited tumors’ bioluminescence at the dose of 30 g crude drug/kg. Mechanistically, HDSB11 attenuated the expressions of NLRP3, procaspase-1, caspase-1, PRAP, Bcl-2, and cyclin D1 and downregulated the phosphorylation levels of NF-κB, ERK, JNK, and p38 MAPK. In conclusion, HDSB11 could alleviate cell proliferation and colony formation and induce apoptosis in vitro and tumor growth in vivo, partly via NF-κB and MAPK signaling pathways to suppress NLRP3 expression.


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