Hyperglycemia-induced endothelial endoplasmic reticulum (ER) stress is implicated in the pathophysiology of diabetes and its vascular complications. Procyanidins are enriched in many plant foods and have been demonstrated to exert several beneficial effects on diabetes, cardiovascular and other metabolic diseases. In the present study, we investigated the effect of procyanidin B2 (PCB2), the most widely distributed natural procyanidin, on ER stress evoked by high glucose in endothelial cells (ECs) and the underlying mechanisms. We showed that PCB2 mitigated the high glucose-activated ER stress pathways (PERK, IRE1α and ATF6) in human vascular ECs. In addition, we found that PCB2 attenuated endothelial ER stress via the activation of peroxisome proliferator-activated receptor δ (PPARδ). We demonstrated that PCB2 directly bound to and activated PPARδ. Conversely, GSK0660, a selective PPARδ antagonist, attenuated the suppressive effect of PCB2 on the ER stress signal pathway. Functionally, PCB2 ameliorated the high glucose-impaired endothelium-dependent relaxation in mouse aortas. The protective effect of PCB2 on vasodilation was abolished in the aortas pretreated with GSK0660 or those from the EC-specific PPARδ knockout mice. Moreover, the protective effects of PCB2 on ER stress and endothelial dysfunction required the inter-dependent actions of PPARδ and AMPK. Collectively, we demonstrated that PCB2 mitigated ER stress and ameliorated vasodilation via a PPARδ-mediated mechanism beyond its classic action as a scavenger of free radicals. These findings further highlighted the novel roles of procyanidins in intervening the ER stress and metabolic disorders related to endothelial dysfunction.

ABSTRACT. We investigated the role of galectin 3 in the development and progression of pituitary tumors. We used RNA interference to depress Gal-3 gene expression; MTT and flow cytometry were applied to detect changes in cell proliferation and apoptosis levels in pituitary tumor cells. Expression of apoptosisassociated genes, Bcl-2 and Baxk was analyzed by Western blot. Inhibition of Gal-3 gene expression by RNA interference decreased GH3 cell proliferation and increased cell apoptosis; the expression levels of Gal-3 protein significantly decreased, along with those of Bcl-2, although Bax levels did not change. We conclude that Gal-3 has an important role in pituitary tumor cell proliferation and progression; and it may be useful as a target for the treatment of aggressive pituitary tumors.

Background: Expression of miR‑92b in oral squamous cell carcinoma (OSCC) rat tissue and its effect on the OSCC CAL‑27 cells were investigated. Methods: The study was performed in Qingdao Stomatological Hospital, Qingdao, China on December 2018. Thirty Wistar rats were used to construct models of oral squamous cell carcinoma. CAL‑27 cells trascfected by Lipofectamine 2000 were divided into miR‑92b inhibitor, miR‑NC and blank groups. RT‑qPCR was used for the detection of the expression level of miR‑92b, and MTT and flow cytometry were carried out for the detection of the effect of miR‑92b on the proliferation and apoptosis of CAL‑27 cells, respectively. Results: The expression level of miR‑92b was significantly higher in tumor tissues than that in normal tissues (P<0.001). The miR‑92b inhibitor group had significantly lower proliferation ability but higher apoptosis rate of CAL‑27 cells than the miR‑NC and blank groups. After miR‑92b was downregulated by trans-fecting cells, the expression level of miR‑92b was significantly lower in the miR‑92b inhibitor group than that in the miR‑NC and blank groups. Conclusion: miR‑92b inhibitor can inhibit the proliferation of CAL‑27 cells and promote apoptosis, which provides certain references for clinical treatment. It is expected to be a potential target for treating OSCC.