Fluoride occurrence in geothermal water of fault zone area, Southeast China.

Fluoride (F-) is a common trace component in groundwater, and long-term exposure to high-F- groundwater is harmful to human health. Fluoride concentrations that exceed the World Health Organization guideline for drinking water (1.5 mg/L) have been detected in thermal and non-thermal groundwater from Southeast China, where the causes of the high fluoride occurrence are lack of study. To study the formation and migration mechanism of high fluoride groundwater from Southeast China, we carried out a systemic sampling of water samples in the surrounding area of Heyuan deep fault zone and Zijin-Boluo fault zone, then a comprehensive discussion including water hydrogeochemical, stable isotope composition, as well as hydrogeology analysis was conducted. Fluoride concentrations in geothermal and non-thermal water samples range from 1.11 to 22.76 mg/L and 0.04-8.3 mg/L, respectively. High temperature, alkaline conditions, and the depleted Ca2+ by reverse cation exchange and calcite precipitation would promote the release of fluoride from host rock to geothermal water. The availability of Ca-bearing and F-bearing minerals in host rock causes significant differences in fluoride concentrations between carbonate reservoir and granite reservoir. Hydrochemical diagrams reveal that the composition of groundwater is affected by mixing and that fractures act as the mixing channels in our study area. The addition of cold groundwater limits the fluoride concentrations by lowing temperature and increasing Ca2+ levels of geothermal water. Additionally, the relationship between F- and SiO2 indicates that geothermal water promotes the fluoride enrichment in cold groundwater, especially in confined aquifers which are more susceptible to geothermal water. The direct input of geothermal fluoride and secondary enrichment caused by alkaline condition contribute to the formation of high F- concentrations (7.2-8.3 mg/L) in confined groundwater. Our findings highlight that the natural evolution of geothermal systems in fault zone can result in the formation of geogenic contaminated groundwater.

Astilbin emulsion improves guinea pig lesions in a psoriasis-like model by suppressing IL-6 and IL-22 via p38 MAPK.

Astilbin has anti-inflammatory and immunoregulatory effects, and is frequently used in prescriptions treating psoriasis; however, the mechanism remains to be fully elucidated. In the present study, the effect of an astilbin microemulsion on a psoriasis­like model in guinea pigs was examined, and the underlying mechanism was investigated. The levels of interkeukin (IL)­6, IL­17A and IL­22 were determined using fluorescent reverse transcription­quantitative polymerase chain reaction analysis and enzyme­linked immunosorbent assays. The phosphorylation of p38 and extracellular signal­regulated kinase (ERK)1/2 was detected using western blot analysis. Compared with the untreated control, astilbin significantly ameliorated the lesions induced by propranolol hydrochloride. The effect of astilbin on cytokine levels were cytokine­ and drug­concentration­dependent. At a concentration of 2.22 µM, astilbin decreased the mRNA expression levels of IL­6, IL­17A and IL­22 in lipopolysaccharide (LPS)­induced HaCaT cells by 89, 69.1 and 69.3%, respectively. However, 2.22 µM astilbin had no effect on the protein expression of IL­17A, and decreased the protein expression levels of IL­6 and IL­22 by 79.2 and 49.5%, respectively (P<0.05). At a concentration of 11.10 µM, astilbin decreased the mRNA expression of IL­6, which was significantly induced by LPS, and significantly (P<0.05) decreased the protein expression levels of IL­6 and IL­22. Additionally, astilbin inhibited the LPS­induced activation of phosphorylated p38. These results suggested that astilbin has the potential to be developed into a topical drug for the treatment of psoriasis via the inhibition of inflammatory cytokines.

Paeoniflorin suppressed IL-22 via p38 MAPK pathway and exerts anti-psoriatic effect.

AIMS: The total glucosides of paeony (TGP) are used to treat psoriasis in the clinic. However, its active components and mechanisms are not clear. Paeoniflorin is the main constituent of TGP. Thus, the anti-psoriasis effect of paeoniflorin was studied, and its mechanism was explored. MATERIALS AND METHODS: The effect of paeoniflorin was evaluated using a psoriasis-like model of guinea pigs. The levels of IL-6, IL-17A, IL-22, p38 MAPK, and ERK1/2 in HaCaT cells stimulated by lipopolysaccharide (LPS) were determined using RT-qPCR, enzyme linked immunosorbent assays (ELISAs) and western blot. KEY FINDING: Compared with the control group, the model group showed edema, redness, and lesions in the ear upon stimulation with propranolol hydrochloride, and the Baker Score increased by 7-fold. Paeoniflorin ameliorated the lesion and decreased the Baker Score by 37% (p<0.05). In vitro, paeoniflorin significantly inhibited the mRNA expression of IL-6, IL-17A and IL-22 at both 2.08 and 10.41µM (p<0.01), and paeoniflorin had a marginal effect on the protein expression of IL-17A and IL-6. However, it inhibited the protein expression of IL-22 significantly, with inhibition ratios of 48.5% and 47.8% at 2.08 and 10.41µM, respectively (p<0.05). This effect was achieved by inhibiting the phosphorylation of p38 MAPK. SIGNIFICANCE: The results of this work demonstrated that paeoniflorin is the active components of TGP and support its use as a therapeutic compound for psoriasis therapy.

Vinegar-baked Radix Bupleuri modulates the cell membrane constituents and inhibits the P-gp activity in rat hepatocytes.

BACKGROUND: Vinegar-baked Radix Bupleuri (VBRB) enhances the effects of other drugs on the liver by increasing drug distribution to the liver, but the mechanism of action remains unclear. The present study was designed to determine the effects of VBRB on the membrane permeability, constituents, and P-glycoprotein (P-gp) activity of hepatocyte BRL cells, in order to interpret the liver targeting enhancing effects of VBRB. METHODS: The membrane permeability and P-gp expression were analyzed by flow cytometry. The membrane constituents were determined by an automatic biochemistry analyzer and thin-layer chromatography. RESULTS: The results showed that, compared with the control, VBRB enhanced the membrane permeability by 41-67% (P < 0.05), which occurred in the absence of any cytotoxicity. VBRB had marginal effects on the cholesterol content, but significantly affected the total protein contents and the lipid constituents of the cell membrane in a dose- and time-dependent manner. VBRB inhibited P-gp expression in the cell membrane by 59-86% (P < 0.01). CONCLUSION: VBRB affects the constituents of BRL cells and increases its permeability, which may help explain its liver-targeting effects.