No abstract

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 (β-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, β-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.

No abstract

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 β-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-β1, and C-myc), as well as their protein expression levels, were associated with the aberrant expression or/and nucleus localization of β-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 β-catenin which in turn plays an important role in the initiation and promotion of liver tumors.