Protective effects of tenuifolin isolated from Polygala tenuifolia Willd roots on neuronal apoptosis and learning and memory deficits in mice with Alzheimer's disease.

The roots of Polygala tenuifolia Willd have a long history of being used as a traditional Chinese medicine for the treatment of insomnia, forgetfulness, sorrow and depression. Tenuifolin (TEN) has been isolated from Polygala tenuifolia Willd roots, and this study was carried out to investigate the potential beneficial effects of TEN on neuronal apoptosis and memory deficits in a mouse model of Alzheimer's disease (AD). TEN treatment reversed spatial learning and memory deficits, as well as neuronal apoptosis in hippocampal areas, in APP/PS1 transgenic AD mice. TEN treatment protected against Aß25-35-induced apoptosis, loss of mitochondria-membrane potential, and activation of caspases-3 and -9 in SH-SY5Y cells. TEN has potential benefit in treating learning and memory deficits in APP/PS1 transgenic AD mice, and its effects may be associated with reversing AD pathology-induced neuronal apoptosis. These insights pave the way for further analysis of the potential of TEN as an AD therapeutic agent.

[Clinical study of modified Gow-Gates technique of inferior alveolar nerve block in impacted mandibular third molar extraction].

PURPOSE: To introduce a minimally invasive and more effective technique of inferior alveolar nerve block. METHODS: Two hundred and six patients who needed extraction of the impacted mandibular third molar were divided randomly into 2 groups: the experimental group (105 cases) with modified Gow-Gates technique (modified Gow-Gates group) and the control group (101 cases) with Halstead technique (Halstead group). The anesthetic success rates, effects and complications were recorded and analyzed with SPSS17.0 software package. RESULTS: The anesthetic success rate was 97.15% in modified Gow-Gates group and 89.10% in Halstead group with significant difference between the 2 groups (P=0.038<0.05); In comparing the anesthesia grade, the ration of grade A and B accounted for 90.48% in modified Gow-Gates group and 87.13% in Halstead group (P=0.446>0.05). Modified Gow-Gates group had much fewer of complications than Halstead group (P=0.014<0.05). CONCLUSIONS: Modified Gow-Gates technique is a minimally invasive and more effective technique for inferior alveolar nerve block anesthesia. Supported by Science and Technology Planning Project of Yueqing City (2014y027).

Toxicity of oxidized beta-carotene to cultured human cells.

Carotenoids are effective antioxidants in vitro, but they are also susceptible to autoxidation, which generates volatile and biologically active aldehydes and ketones. In a previous study, we showed that autoxidized beta-carotene inhibits Na+-K+-ATPase activity more effectively than aldehydic products derived from lipid peroxidation, such as 4-hydroxynonenal. In this study, we compared mitochondrial dysfunction in cultured human K562 erythroleukaemic and 28 SV4 retinal pigment epithelium (RPE) cells in response to the degradation products of beta-carotene autoxidation using the MTT assay. We found that oxidized beta-carotene is cytotoxic and that mitochondrial function is decreased in both K562 and RPE cells. In addition, the RPE cells were more resistant to this form of oxidative stress, suggesting that its cytotoxicity may depend on cellular antioxidant capacity.

Gastrin stimulates cyclooxygenase-2 expression in intestinal epithelial cells through multiple signaling pathways. Evidence for involvement of ERK5 kinase and transactivation of the epidermal growth factor receptor.

Gastrin is a hormone produced by G-cells in the normal gastric antrum. However, colorectal carcinoma cells may aberrantly produce gastrin and exhibit increased expression of cholecystokinin B (CCK-B)/gastrin receptors. Gastrin is trophic for the normal gastric oxyntic mucosa and exerts a growth-promoting action on gastrointestinal malignancy. Thus, gastrin may act as an autocrine/paracrine or endocrine factor in the initiation and progression of colorectal carcinoma. The molecular mechanisms involved have not been elucidated. Hypergastrinemia induced by Helicobacter pylori infection is associated with increased cyclooxygenase-2 (COX-2) expression in gastric and colorectal tissues, suggesting the possibility that gastrin up-regulates COX-2 expression in these tissues; this has not been confirmed. We report here that gastrin significantly increases the expression of COX-2 mRNA and protein, the activity of the COX-2 promoter, and the release of prostaglandin E(2) from a rat intestinal epithelial cell line transfected with the CCK-B receptor. These actions were dependent upon the activation of multiple MAPK signal pathways, including ERK5 kinase; transactivation of the epidermal growth factor receptor; and the increased expression and activities of transcription factors ELK-1, activating transcription factor-2, c-Fos, c-Jun, activator protein-1, and myocyte enhancer factor-2. Thus, our findings identify the signaling pathways coupling the CCK-B receptor with up-regulation of COX-2 expression. This effect may contribute to this hormone-dependent gastrointestinal carcinogenesis, especially in the colon.

Bcl-2 overexpression increases survival in human retinal pigment epithelial cells exposed to H(2)O(2).

The integrity of the retinal pigment epithelium, especially that of the macula is essential for the preservation of vision into old age. The chronic exposure to sunlight and peroxidized lipids from phagocytized photoreceptor outer segments imposes a high level of oxidative stress on the retinal tissues, which increases with age as antioxidant protection declines and therefore could accelerate apoptosis. Bcl-2 known to facilitate mitochondrial DNA repair and cellular survival in other tissues was overexpressed in a single clone of human retinal pigment epithelium cells after stable transfection with humanbcl-2 in rhoSFV-neoexpression factor. Near confluent cells (2nd-4th generation permanently bcl-2 transfected) were protected from mitochondrial dysfunction after exposure to H(2)O(2) up to 150 microM. With 200 microM H(2)O(2), function in transfected cells declined by only 25% control activity as determined by MTT reduction assays, compared to wild type and vector only transfected cells expressing normal bcl-2 levels. Similarly the bcl-2 -transfected cells were more resistant to mitochondrial DNA damage after H(2)O(2) treatment than the other groups and suffered 50% less damage after exposure to 200 microM H(2)O(2), as assayed by quantitative polymerase chain reaction assays. These data suggest that bcl-2 overexpression protects human RPE cells from mitochondrial respiratory dysfuction, mitochondrial DNA damage and promotes cellular survival in response to oxidative stress induced by H(2)O(2).