Objective: To determine the cytotoxicity, reduction in nitric oxide production and anti-oxidative activity of the aqueous leaf extract from Tithonia diversifolia (T. diversifolia) in an in vitro model.
Methods: Leaves of T. diversifolia were collected from natural habitats and extracted with distilled water using the decoction method. The cytotoxic effect of the extract in terms of cell viability was determined using RAW264.7 cells and human peripheral blood mononuclear cells (PBMCs) via the mitochondrial respiration method using the MTT reagent. The effect of the extract on lipopolysaccharide (LPS)-induced nitric oxide pro-duction in RAW264.7 cells was measured using the Griess reagent. The chemical anti-oxidant was evaluated by ABTS-and DPPH-radical scavenging assays.
Results: The half-maximal cytotoxic concentration values were 145.87 mg/mL and 73.67 mg/mL for human PBMCs and RAW264.7 cells, respectively. In the presence of phytohemagglutinin-M, the IC50 on PBMCs proliferation was 4.42 mg/mL. The non-cytotoxic range of the extracts inhibited LPS-induced nitrite production in RAW264.7 cells with an IC50 value of 11.63 mg/mL. To determine the anti-oxidative properties, the N-acetyl cysteine equivalent antioxidant capacity of the extract was (32.62 ± 1.87) and (20.99 ± 2.79) mg N-acetyl cysteine/g extract, respectively determined by the ABTS-radical and DPPH-radical assay. However, the extract did not confer death protection in a hydrogen peroxide-induced RAW264.7 co-culturing model.
Conclusions: Our study demonstrated the immunomodulation caused by the aqueous leaf extract of T. diversifolia, resulting from the inhibition of phytohemagglutinin-M-induced PBMCs proliferation and LPS-induced nitric oxide production in RAW264.7 macrophages. Although the anti-oxidative activity was presented in the chemical-based anti-oxidant assay, the extract cannot protect cell death from stress conditions.

Objective To determine the cytotoxicity, reduction in nitric oxide production and anti-oxidative activity of the aqueous leaf extract from Tithonia diversifolia (T. diversifolia) in an in vitro model. Methods Leaves of T. diversifolia were collected from natural habitats and extracted with distilled water using the decoction method. The cytotoxic effect of the extract in terms of cell viability was determined using RAW264.7 cells and human peripheral blood mononuclear cells (PBMCs) via the mitochondrial respiration method using the MTT reagent. The effect of the extract on lipopolysaccharide (LPS)-induced nitric oxide production in RAW264.7 cells was measured using the Griess reagent. The chemical antioxidant was evaluated by ABTS- and DPPH-radical scavenging assays. Results The half-maximal cytotoxic concentration values were 145.87 μg/mL and 73.67 μg/mL for human PBMCs and RAW264.7 cells, respectively. In the presence of phytohemagglutinin-M, the IC

Wax apple (Syzygium samarangense) has received growing research interest for its high nutritional and medicinal value due to its constituents such as polysaccharide, organic acids, flavonoids, minerals, and other substances. In this study, wax apple polysaccharide (WAP) was isolated from this plant and its protective effect against ethyl carbamate (EC)‍-induced oxidative damage was evaluated in human hepatocytes (L02 cells). Firstly, a series of analyses such as high-performance liquid chromatography (HPLC), high-performance gel permeation chromatography (HPGPC), Fourier transform infrared spectroscopy (FT-IR), gas chromatography/mass spectrometry (GC/MS), and ¹H and ¹³C nuclear magnetic resonance (NMR) were conducted to identify the structure of WAP. Thereafter, in vitro cell experiments were performed to verify the protective effects of WAP against EC-induced cytotoxicity, genotoxicity, and oxidative damage in L02 cells. Our results revealed that WAP is composed of mannose, rhamnose, glucuronic acid, galacturonic acid, glucose, galactose, arabinose, and fucose in a molar ratio of 2.20:‍3.94:‍4.45:‍8.56:‍8.86:‍30.82:‍39.78:‍1.48. Using a combination of methylation and NMR spectroscopic analysis, the primary structure of WAP was identified as Araf-(1→, Glcp-(1→, →2)‍-Araf-(1→, →3)‍-Galp-(1→, →3)‍-Araf-‍(1→, and →6)‍-Galp-‍(1→. Cell experiments indicated that WAP exhibited significant protective effects on EC-treated L02 cells via suppressing cytotoxicity and genotoxicity, reducing reactive oxygen species (ROS) and O₂^•- formation, as well as improving mitochondrial membrane potential (MMP) and glutathione (GSH). In a nutshell, WAP has the potential as an important therapeutic agent or supplement for hepatic oxidative damage. Meanwhile, further studies are needed to prove the above effects in vivo at the biological and clinical levels.
Humans ; Syzygium/chemistry* ; Urethane/pharmacology* ; Spectroscopy, Fourier Transform Infrared ; Oxidative Stress ; Glutathione/pharmacology* ; Hepatocytes ; Polysaccharides/pharmacology*