Influenza is an acute transmissible respiratory infectious disease in humans and animals with high morbidity and mortality. It was reported that luteolin, extracted from Chinese herbs, could potently inhibit influenza virus replication in vitro. To assess the effect and explore the fundamental mechanism of luteolin, we infected several cell lines with two subtypes of influenza A virus (IAV), including A/Jiangxi/312/2006 (H3N2) and A/Fort Monmouth/1/1947 (H1N1) and demonstrated that luteolin suppressed the replication of IAV by cytopathic effect reduction method, qRT-PCR, immunofluorescence and Western blot assays. A time-of-addition assay indicated that this compound interfered with viral replication at the early stage of infection. In addition, we found that luteolin suppressed coat protein I complex expression, which was related to influenza virus entry and endocytic pathway. Overall, our findings demonstrated the antiviral effect of luteolin against IAV and its novel antiviral mechanism.
Nymphaea candida was used to treat hepatitis in Ugyhur medicine, and nicotiflorin (kaempferol 3-O-β-rutinoside) is the main characteristic component in this plant. In this study, The the hepatoprotective activities of nicotiflorin from N. candida were investigated by Concanavalin A (Con A, 20 mg/kg bw)-and D-Galactosamine (D-GalN, 800 mg/kg bw)-induced acute liver injury in mice. Pretreatment with nicotiflorin (25, 50, 100 mg/kg bw/day, p.o.) for ten days significantly reduced the impact of Con A toxicity (20 mg/kg bw) on the serum markers of liver injury, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). The hepatic anti-oxidant parameters (malondialdehyde, MDA; superoxide dismutase, SOD; glutathione, GSH; and nitric oxide, NO) in mice with nicotiflorin treatment were significantly antagonized for the pro-oxidant effects of Con A. Moreover, pretreatment with nicotiflorin (100 mg/kg bw) significantly decreased Con A-induced elevation in the serum levels of pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) (p < 0.05). A protective effect was reconfirmed against D-GalN-induced chemical liver injury, elevated serum enzymatic and cytokines levels were significantly decreased by nicotiflorin, and liver homogenate antioxidant indicators were significantly restored toward normal levels. Both histopathological studies also supported the protective effects of nicotiflorin. Therefore, the presented results suggest that nicotiflorin is the potent hepatoprotective agent that could protect the liver against acute immunological and chemical injury; this ability might be attributed to its antioxidant and immunoregulation potential.
Nigella glandulifera seeds are used as a spice or remedy for the treatment of various inflammatory diseases. This study aimed to investigate analgesic (writhing test), anti-inflammatory (ear-induced edema, vascular permeability test), antioxidant, and antitumor activities of total saponins from this plant (TSN). TSN (6, 12, and 24 mg/kg) were exhibited analgesic and anti-inflammatory activities in a dose-dependent manner (P < 0.05). In D-galactose-induced ageing model, TSN significantly increased the plasma superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities (P < 0.05) and decreased the malondialdehyde (MDA) level compared to control group (P < 0.05). DPPH radical scavenging effect of TSN was also found. Moreover, TSN (20 mg/mL) showed 86.75% and 88.26% inhibition of the growth on Bel-7402 and Hela cells, respectively. Five compounds were further isolated and identified from TSN as Nigella A, B, C, D, and nigeglanoside, of which the content of Nigella A was 60.36 ± 1.25 g/100 g TSN by HPLC-ELSD method. Altogether, these results suggest that TSN could be considered as a potential analgesic, anti-inflammatory, antitumor, and antioxidant agent.
The hepatoprotective effects of acteoside from O. coerulescens were evaluated in BCG plus LPS-induced immunological liver injury (ILI) in mice. Acteoside (50, 150, or 300 mg/kg) was administered via gavage daily for 12 days. The liver index (liver weight/body weight), liver homogenate levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), hepatic nitric oxide (NO), malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, production of tumor necrosis factor-gamma (TNF-gamma) and interleukin-2, 4, 10 (IL-2, 4, 10), as well as histopathological changes of the liver were evaluated following the 12-day treatment. Moreover, the modulation influence of acteoside on the expression of B cell lymphoma/leukemia-2 (Bcl-2, hepatocyte apoptosis inhibitor) and Bcl-2 associated X protein (Bax, hepatocyte apoptosis promoter) in the mice liver with immunological hepatic injury was studied also. Acteoside (50, 150, or 300 mg/kg) effectively reduced the BCG/LPS-induced elevated liver index, liver homogenate AST and ALT levels, hepatic NO and MDA contents, restored hepatic SOD activity and reduced the degree of liver injury in ILI mice. The expression of Bax was decreased (vs. BCG + LPS model group), while the expression of Bcl-2 increased (vs. BCG + LPS model group). These results are close to those of DDB (as a reference drug), and suggest that acteoside has a protective and therapeutic effect on ILI mice, which might be associated with its antioxidant properties, immunoregulatory function and regulation of hepatic apoptosis.
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