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To study the chemical constituents of Pteris ensiformis, silica gel, gel, MCI, C18 and other column chromatography were used for separation and purification, and their structures were identified by 1H-NMR, 13C-NMR, MS, IR and othe spectral data; the anti-tumor and anti-coagulation activities of some monomers were screened by MTS, APTT, PT and TT. The results were as follows: (1) A total of 15 compounds were isolated from P. ensiformis, the compounds were 2-hydroxy-acetylpyrrole (1), N-(3-carboxypropyl)-2-acetylpyrrole (2), 3-hydroxy-2-methylpyridine (3), N-methylhydroxylamine (4), pterosin S 13-O-glucoside (5), obtupterosin C (6), ent-11α-hydroxy-15-oxokauran-19-oic acid (7), ent-11α-hydroxy-15-oxokaur-16-en-19-oic acid (8), β-sitosterol (9), ent-11α-hydroxy-15-oxokaur-16-en-19-oic acid-O-glucopyranoside (10), 5, 5′-dibutoxy-2, 2′-bifuran (11), 5, 5′-di (2-ethyl-hexyloxy)-2, 2′-bifuran (12), (-)-loliolide (13), succinic acid (14), fumaric acid (15). Compound 1 is a new natural product of pyrrole alkaloids. Compounds 1-7, 10-15 were isolated from P. ensiformis for the first time, and compounds 1, 3, 4 were isolated from Pteris for the first time. (2) The results of activity test showed that compounds 1, 2, 3, 5, 6 and 10 inhibited the growth of tumor cells HL-60, A549, SMMC-7721, MDA-MB-231 and SW480 in vitro at a concentration of 40 μmol·L-1, At the concentration of 2.0 mmol·L-1, compounds 1, 2, 3 and 6 shortened APTT and compounds 1, 5 and 6 prolonged PT. The study enriches the chemical constituents of P. ensiformis from Guizhou and provides a material basis for the development of anti-tumor drugs.

Based on the literature review, this paper summarized the Traditional Chinese Medicine nursing of peptic ulcer bleeding from perspectives of emergency care, routine nursing and comprehensive nursing management, and provided reference for the improvement of Traditional Chinese Medicine nursing protocol for peptic ulcer bleeding. (本文通过查阅文献, 从急救护理、常规护理、综合护理等各方面对消化性溃疡出血的中医护理进行了综述, 以期为进一步完善消化性溃疡并出血的中医护理方案提供参考。)

Statins are cholesterol-lowering agents that increase the incidence of diabetes and impair glucose tolerance via their detrimental effects on nonhepatic tissues, such as pancreatic islets, but the underlying mechanism has not been determined. In atorvastatin (ator)-treated high-fat diet-fed mice, we found reduced pancreatic β-cell size and β-cell mass, fewer mature insulin granules, and reduced insulin secretion and glucose tolerance. Transcriptome profiling of primary pancreatic islets showed that ator inhibited the expression of pancreatic transcription factor, mechanistic target of rapamycin (mTOR) signaling, and small G protein (sGP) genes. Supplementation of the mevalonate pathway intermediate geranylgeranyl pyrophosphate (GGPP), which is produced by 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, significantly restored the attenuated mTOR activity, v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) expression, and β-cell function after ator, lovastatin, rosuvastatin, and fluvastatin treatment; this effect was potentially mediated by sGP prenylation. Rab5a, the sGP in pancreatic islets most affected by ator treatment, was found to positively regulate mTOR signaling and β-cell function. Rab5a knockdown mimicked the effect of ator treatment on β-cells. Thus, ator impairs β-cell function by regulating sGPs, for example, Rab5a, which subsequently attenuates islet mTOR signaling and reduces functional β-cell mass. GGPP supplementation could constitute a new approach for preventing statin-induced hyperglycemia. [ABSTRACT FROM AUTHOR]

Statins are cholesterol-lowering agents that increase the incidence of diabetes and impair glucose tolerance via their detrimental effects on nonhepatic tissues, such as pancreatic islets, but the underlying mechanism has not been determined. In atorvastatin (ator)-treated high-fat diet-fed mice, we found reduced pancreatic β-cell size and β-cell mass, fewer mature insulin granules, and reduced insulin secretion and glucose tolerance. Transcriptome profiling of primary pancreatic islets showed that ator inhibited the expression of pancreatic transcription factor, mechanistic target of rapamycin (mTOR) signaling, and small G protein (sGP) genes. Supplementation of the mevalonate pathway intermediate geranylgeranyl pyrophosphate (GGPP), which is produced by 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, significantly restored the attenuated mTOR activity, v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) expression, and β-cell function after ator, lovastatin, rosuvastatin, and fluvastatin treatment; this effect was potentially mediated by sGP prenylation. Rab5a, the sGP in pancreatic islets most affected by ator treatment, was found to positively regulate mTOR signaling and β-cell function. Rab5a knockdown mimicked the effect of ator treatment on β-cells. Thus, ator impairs β-cell function by regulating sGPs, for example, Rab5a, which subsequently attenuates islet mTOR signaling and reduces functional β-cell mass. GGPP supplementation could constitute a new approach for preventing statin-induced hyperglycemia., (© 2019 by the American Diabetes Association.)