Shengfu Oil Enhances the Healing of Full-Thickness Scalded Skin Accompanying the Differential Regulation of ß-Catenin, Dlk1, and COX-2.

Shengfu oil is a traditional Chinese medicine formula containing 16 ingredients, including Scutellariae radix, Olibanum, and Rehmanniae radix. In this study, we aimed to enhance the wound healing of rabbit full-thickness scalded skin by Shengfu oil and to elucidate its regulatory effects on ß-catenin, Dlk1, and COX-2. We found that Shengfu oil exhibited significant anti-inflammatory, analgesic, and antimicrobial activities. The structure of wound tissues in Shengfu oil group was intact, including regenerated cutaneous appendages, indicating better healing capability of Shengfu oil compared to the controls. The protein expression of ß-catenin, Dlk1, and COX-2 in wound tissues were investigated by immunohistochemistry staining and were further quantitated with the use of multispectral imaging analysis. The protein expression of ß-catenin and Dlk1 in the Shengfu oil group was higher than that in the sesame oil group in early wound repair, accompanied by the lower expression of COX-2; the protein expression of ß-catenin decreased in the middle of wound healing; the protein expression of ß-catenin and Dlk1 increased at the end of wound healing. These results strongly suggest that Shengfu oil can enhance wound healing by regulating the expression of ß-catenin, Dlk1, and COX-2 due to its excellent anti-inflammatory, analgesic, and antimicrobial activities.

Electroacupuncture Treatment Alleviates Central Poststroke Pain by Inhibiting Brain Neuronal Apoptosis and Aberrant Astrocyte Activation.

Electroacupuncture (EA) is reported to effectively relieve the central poststroke pain (CPSP). However, the underlying mechanism remains unclear. The present study investigated the detailed mechanisms of action of EA treatment at different frequencies for CPSP. A CPSP model was established with a single collagenase injection to the left ventral posterolateral nucleus of the thalamus. The EA-treated groups then received EA treatment at frequency of 2, 2/15, or 15 Hz for 30 min daily for five days. The pain-related behavioral responses, neuronal apoptosis, glial activation, and the expression of pain signal transmission-related factors (ß-catenin, COX-2, and NK-1R) were assessed using behavioral tests, Nissl staining, TUNEL staining, and immunohistochemical staining, respectively. The low-frequency EA treatment significantly (1) reduced brain tissue damage and hematoma sizes and (2) inhibited neuronal apoptosis, thereby exerting abirritative effects. Meanwhile, the high-frequency EA treatment induced a greater inhibition of the aberrant astrocyte activation, accompanied by the downregulation of the expressions of COX-2, ß-catenin, and subsequently NK-1R, thereby alleviating inflammation and producing strong analgesic effects. Together, these findings suggest that CPSP is closely related to pathological changes of the neocortex and hippocampus. EA treatments at different frequencies may exert abirritative effects by inhibiting brain neuronal apoptosis and aberrant astrocyte activation in the brain.

Mouse hepatic neoplasm formation induced by trace level and low frequency exposure to diethylnitrosamine through ß-catenin signaling pathway.

It has been reported that massive levels or/and high frequency exposure of diethylnitrosamine could induce hepatic neoplasm. However, it would be more interesting to figure out the hepatotoxic effects of diethylnitrosamine exposure at trace level and low frequency, which could be more common in our daily life. We found that both the mRNA and protein expression levels of ß-catenin were aberrant in all liver tissues, accompanied by inflammation, steatosis, fibrosis and hepatic neoplasm after 10-week exposure of diethylnitrosamine (dissolved in sesame oil, 0.16 mmol per kg body weight) to mice. In addition, gradual increase in the mRNA expression of several pivotal risk factors (TNF-α, COX-2, PPAR-γ, AP-2, Smad-2, TGF-ß1, and C-myc), as well as their protein expression levels, were associated with the aberrant expression or/and nucleus localization of ß-catenin. Altogether, our results show that long-term diethylnitrosamine exposure at trace amounts and low frequency can also induce hepatotoxicity (including inflammation, steatosis and fibrosis) and consequently aberrant activation of ß-catenin which in turn plays an important role in the initiation and promotion of liver tumors.

[Efficient oxidative degradation of tetrabromobisphenol A by silver bismuth oxide].

Silver bismuth oxide(BSO) was prepared by a simple ion exchange-coprecipitation method with AgNO3 and NaBiO, .2H2O as raw materials, and then used to oxidatively degrade tetrabromobisphenol A(TBBPA). Effects of the molar ratio of Ag/Bi during BSO preparation and the BSO dosage on the degradation of TBBPA were investigated. The results showed that under the optimized conditions (i.e., the Ag/Bi molar ratio of 1:1, BSO dosage of 1 g x L(-1), 40 mg x L(-1) of TBBPA was completely degraded and the removal of total organic carbon achieved more than 80% within 7 min. The degradation intermediates of TBBPA were identified by ion chromatography, gas chromatograph-mass spectrometer and X-ray photoelectron spectroscopy. The degradation pathway of TBBPA included the debromination, the cleavage of tert-butyl group and the open epoxidation of benzene ring. Based on a quenching study of NaN3, singlet oxygen was proved to play a dominant role in the TBBPA degradation.