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1.
J Asian Nat Prod Res ; 22(8): 732-737, 2020 Aug.
Article in English | MEDLINE | ID: mdl-31154855

ABSTRACT

Two new flavonoids, 5,4'-dihydroxy-6,7-furanbavachalcone (1), 1″-methoxy-6,7-furanflavanone (2), together with five known compounds (3-7), were isolated from the seeds of Psoralea corylifolia. Their structures were elucidated by IR, UV, NMR, HRESMS experiments, and comparison of their NMR data with previously reported data. All compounds were evaluated for in vitro inhibitory activity against PTP1B. Additionally, the isolated compounds (1-6) displayed moderate inhibitory effects against PTP1B with IC50 values ranging from 10.3 ± 0.9 to 25.1 ± 1.6 µM.


Subject(s)
Protein Tyrosine Phosphatase, Non-Receptor Type 1 , Psoralea , Flavonoids , Molecular Structure , Seeds
2.
J Cell Biochem ; 120(2): 1754-1762, 2019 Feb.
Article in English | MEDLINE | ID: mdl-30160788

ABSTRACT

The pathogenic mechanism of autism is complex, and current research has shown that long noncoding RNAs (lncRNAs) may play important roles in this process. The antisense lncRNA of SH3 and multiple ankyrin repeat domains 2 (Shank2-AS) is upregulated in patients with autism spectrum disorder (ASD), whereas the expression of its sense strand gene Shank2 is downregulated. In neuronal cells, Shank2-AS and Shank2 can form a double-stranded RNA and inhibit Shank2 expression. Overexpression of Shank2-AS decreases neurite numbers and lengths, thereby inhibiting the proliferation of neuronal cells and promoting their apoptosis. Overexpression of Shank2 inhibits the abovementioned effects of Shank2-AS, and transfection of a vector containing the 10th intron of Shank2 (Shank2-AS is reverse-transcribed from this region) also blocks the function of Shank2-AS. Shank2 small interfering RNA plays a role similar to Shank2-AS. Therefore, Shank2-AS is abnormally expressed in patients with ASD and may affect the structure and growth of neurons by regulating Shank2 expression, thereby facilitating the development of ASD.

3.
Oral Surg Oral Med Oral Pathol Oral Radiol ; 121(4): 381-389.e1, 2016 Apr.
Article in English | MEDLINE | ID: mdl-26972538

ABSTRACT

OBJECTIVE: Currently, there is no consensus on the effect of coffee consumption on the risk of oral cancer. We performed a meta-analysis based on published studies to uncover the association. STUDY DESIGN: We searched PubMed (1946-2015), Embase (1976-2015), and the bibliographies of all retrieved articles for relevant citations. We performed random-effects meta-analyses of observational studies on coffee consumption and oral cancer. RESULTS: A total of 11 case-control studies and 4 cohort studies comprising 2,832,706 controls and 5021 cases of oral cancer were included in our analysis. The results indicated that the summary odds ratio for the highest versus the lowest or no category consumption of coffee was 0.63 (95% confidence interval [CI]: 0.52-0.75). The odds ratios were 0.60 (95% CI: 0.49-0.74) for case-control studies and 0.66 (95% CI: 0.45-0.98) for cohort studies. CONCLUSION: Overall, our results suggested that coffee consumption appears to have a protective benefit in oral cancer.


Subject(s)
Coffee , Mouth Neoplasms/prevention & control , Humans , Risk Factors
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