Amelioration of TPA-induced skin inflammation by the leaf extract of Vernonia amygdalina involves ERK/STAT3 (Ser727) signaling inhibition.

BACKGROUND: Uncontrolled inflammation causes health problems. Extracellular signal-regulated kinase (ERK) phosphorylates signal transducer and activator of transcription 3 (STAT3) at Ser727, resulting in inflammation. The leaf of Vernonia amygdalina (VA) is a medicinal herb for managing inflammation-associated diseases. Oral administration or topical application of VA leaf extract exerts anti-inflammatory effects in rat models. However, the anti-inflammatory mechanisms of the herb are not fully understood. PURPOSE: In this study, we aimed to investigate the involvement of ERK/STAT3 (Ser727) signaling in the anti-inflammatory effects of an ethanolic extract of VA leaves. STUDY DESIGN AND METHODS: Extracts of VA leaves were prepared with different concentrations of ethanol. A LPS-stimulated RAW264.7 cell model was used for in vitro assays, and a TPA (12-O-tetradecanoylphorbol-13-acetate)-induced ear edema mouse model was employed for in vivo assays. The 95% ethanol extract of VA leaves (VAE) exerted the strongest inhibitory effect on nitric oxide (NO) production in LPS-stimulated macrophages; thus it was selected for use in this study. Hematoxylin and eosin (H&E) staining was used to examine pathological conditions of mouse ear tissues. Griess reagent was employed to examine NO generation in cell cultures. Immunoblotting and ELISA were used to examine protein levels, and RT-qPCR was employed to examine mRNA levels. RESULTS: Topical application of VAE ameliorated mouse ear edema induced by TPA. VAE suppressed the phosphorylation of ERK (Thr202/Tyr204) and STAT3 (Ser727); and decreased protein levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin (IL)-6, IL-1ß and tumor necrosis factor-α (TNF-α) in the mouse ear tissues and in LPS-stimulated RAW 264.7 cells. VAE also inhibited NO production, and lowered mRNA levels of IL-6, IL-1ß and TNF-α in the macrophages. CONCLUSIONS: VAE ameliorates TPA-induced mouse ear edema. Suppression of ERK/STAT3 (Ser727) signaling is involved in VAE's anti-inflammatory effects. These novel data provide further pharmacological justifications for the medicinal use of VA in treating inflammation-associated diseases, and lay the groundwork for developing VAE into a new anti-inflammatory agent.

[Effects of polymer aluminum hydrolysis on phosphorus distribution in coagulation].

Coagulation treatment was conducted by using coagulants of different basicity (ratio of OH(-)/Al); contents,distributions and algal availability of phosphorus in water were studied before and after coagulation. Results show that: phosphorus removals and its distribution in water were markedly different according to the coagulant with different basicity used; Al(a) plays an important role in the coagulation experiment for P removal. The lower the coagulant basicity was, the higher phosphorus removal was achieved; and PACl0 showed the best performance. Dissolved and particulate phosphorus reduced gradually with the increase of the coagulant (PACl0). They were entirely turned into deposit phosphorus when the coagulant dosage was above 10 mg x L(-1). The demand of coagulant for turbidity control was proved to be unequal to that for phosphorus removal. The coagulant dosages of about 3-5 mg x L(-1) achieved the best turbidity removal in the experiment; while much higher dosage was needed to get desired phosphorus removal. The amount of AAP (algal available phosphorus) in the sediments changed according to coagulant (PAC10) dosages. AAP increased with the increase of coagulant dosage when the dosage was less than 5 mg x L(-1), then it decreased with further addition of coagulant above 5 mg x L(-1). It was proved that release of phosphorus in sediments would be controlled effectively by addition of coagulant overdosed compared to the need for turbidity removal, which is important to long-term control of phosphorus. It was indicated that the dosage of coagulant used for phosphorus removal can not use the sole criterion for turbidity removal; the need for total phosphorus removal, sediment release of available phosphorus (such as AAP) and other phosphorus control requirements should be considered; and a larger dosage would be needed.