Simultaneous identification and analysis of cassane diterpenoids in Caesalpinia minax Hance by high-performance liquid chromatography with quadrupole time-of-flight mass spectrometry.

Cassane diterpenoids were successfully and simultaneously identified in Caesalpinia minax Hance by high-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry. A total of 59 peaks were detected, and among them 51 compounds, including 41 furanocassane diterpenoids, 10 furanolactone cassane diterpenoids were simultaneously identified and characterized on the basis of the protonated molecule, retention behavior, and fragments in MS(2) . Ten compounds, including seven novel compounds, were identified or tentatively identified for the first time in C. minax. In a positive ion mode, the fragmentation pathways of cassane diterpenoids were also analyzed for the first time. The relative amounts of the five main diterpenoids (caesalpinin L, caesalpinin F2 , bondcellpin C, caesalpinin E, and ξ-caesalmin) were simultaneously quantified by high-performance liquid chromatography. Results showed that the newly discovered and known components of C. minax can be used to determine the material basis of bioactivity; this method can also be applied to analyze cassane diterpenoids in herbal medicines from the genus Caesalpinia belonging to the family Fabaceae.

Effects of dietary wild bitter melon (Momordica charantia var. abbreviate Ser.) extract on glucose and lipid metabolism in HFD/STZ-induced type 2 diabetic rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Plant-based extracts to interfere with the onset of diabetes may be a promising approach towards type 2 diabetes mellitus (T2DM). Bitter gourd (Momordica charantia L.) is popularly consumed as an edible and medicinal resource with hypoglycemic effect in China. Wild bitter gourd (Momordica Charantia var. abbreviata Ser.) is a variant of bitter gourd, but there are relatively few studies on it. AIM OF THE STUDY: The purpose of the experiment is to first screen out the most effective extraction part of Momordica charantia L. and Momordica Charantia var. abbreviata Ser. through the hypoglycemic activity experiment in vitro, and by using a high-fat and high-sugar diet with STZ-induced diabetic rat model in vivo to explore the possible mechanism of action against diabetes. MATERIALS AND METHODS: This study first performed α-glucosidase, PTP1B and lipase activities inhibition experiments on the alcohol and water extracts of Momordica charantia L. and Momordica Charantia var. abbreviata Ser. Sprague Dawley rats were either given normal feed or a high sugar and fat diet for four weeks, followed STZ (25 mg/kg, via i. p.) was given. Rats with fasting blood glucose ≥11.1 mmol/l after one week were deemed to be diabetic, treatments were administered for four weeks, and then blood samples were used to evaluate hematological and biochemical indicators, and liver was removed for post-analysis. The expression levels of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, AKT, p-GSK3ß, GSK3ß, p-IRS-1, IRS-1, GLUT2 were determined by Western blot. At the same time, the chemical components was identified by liquid-mass spectrometry. RESULTS: Data showed that the ethanol extract of wild bitter gourd (WBGE) had the best ability to regulate glucose and lipid metabolism in vitro. Therefore, we further investigated the antidiabetic effects of oral consumption of WBGE on high-fat diet (HFD) and streptozotocin (STZ)-induced T2DM in SD rats. WBGE effectively reduced blood glucose and lipid levels, alleviated glucose intolerance and insulin resistant. Moreover, WBGE consumption could also inhibited oxidant responses and inflammatory damage. Mechanism studies have shown that WBGE may act by regulating AMPK/PI3K signaling pathway. On the other hand, the content of total phenol, total flavonoids, total saponins and total polysaccharide were measured by UV, 27 compounds were identified by LC-MS. CONCLUSIONS: These studies explored the role and mechanism of WBGE in regulating glucose and lipid metabolism, and may support the utilization and further investigation of wild bitter gourd as a dietary intervention strategy to prevent diabetes and related metabolic abnormalities.

Hypoglycemic Effects of Licochalcone A on the Streptozotocin-Induced Diabetic Mice and Its Mechanism Study.

Type 2 diabetes mellitus (T2DM) is a type of metabolic illness based on relatively insufficient insulin secretion and insulin resistance (IR) as pathophysiological bases. Currently, it is the main type of diabetes. Hypoglycemic and hypolipidemic effects of licochalcone A (LicA) on high-fat diet and streptozocin-caused T2DM were studied. LicA can remarkably decline the IR index and blood glucose and serum lipid levels. Also, the treatment of LicA can improve the "three more and one less" phenomenon in T2DM mice, such as excessive drinking, eating, urine, and weight loss. In addition, LicA can improve oral glucose tolerance, pancreatic injury, and liver enlargement in T2DM mice. Network pharmacology analysis demonstrated that the observed pharmacological effects were mediated by regulating the insulin signal transduction pathway. Therefore, the PI3K/Akt-signaling pathway was selected for verification; it was demonstrated that LicA could improve the insulin-signaling pathway, protect islet cells, improve IR, reduce blood glucose levels, and alleviate lipid metabolism disorder. Its mechanism of influence may be closely related to LicA up-regulating the liver and pancreas IRS-2/PI3K/AKT-signaling pathway. Among them, the high-dose group of LicA had the best effect, which provided an idea for the use of LicA as a nutritional agent in the cure of T2DM.

Protective effect of acorn (Quercus liaotungensis Koidz) on streptozotocin-damaged MIN6 cells and type 2 diabetic rats via p38 MAPK/Nrf2/HO-1 pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Acorn obtained from the Quercus liaotungensis Koidz tree is consumed as a Chinese folk medicine for the treatment of diarrhea, abdominal pain, and inflammation, also having strong antioxidant activity and have been utilized for the treatment of diabetes in China. However, its mechanism of action on complications of diabetes and oxidative stress is unclear. AIM OF THE STUDY: The purpose of this research was to assess the effects of acorn (Quercus liaotungensis Koidz) ethanol extract (AE) on pancreatic ß-cell dysfunction through a streptozotocin (STZ)-damaged mouse normal pancreatic ß-cell (MIN6 cell) model in vitro, and by using a high-fat and high-sugar diet with STZ-induced diabetic rat model in vivo to explore the possible mechanism of action against diabetes. MATERIALS AND METHODS: MIN6 cells were pretreated with AE (20, 40, 80 µM) for 2 h and then treated with 3 mM STZ for 24 h. Cell viability was measured by MTT assay. The amount of intracellular reactive oxygen species was measured by 2,7-dichlorodi-hydrofluorescein diacetate. The activities of insulin secretion, superoxide dismutase, catalase and glutathione were determined by kits. Sprague Dawley rats were either given normal feed or a high sugar and fat diet for four weeks, followed STZ (25 mg/kg, via i. p.) was given. Rats with fasting blood glucose ≥11.1 mmol/l after one week were deemed to be diabetic. Animals were divided into 5 groups, which received saline (10 mL/kg), metformin (200 mg/kg), or AE at doses of 200 and 400 mg/kg during 4 weeks by oral gavage. Blood samples were used to evaluate hematological and biochemical indicators, and pancreas was removed for post-analysis. Body weight and fasting blood glucose were recorded weekly. The expression levels of Bax, Bcl-2, p38, p-p38, Nrf2 and HO-1 were determined by Western blot. RESULTS: Data showed that AE inhibited apoptosis and increased antioxidant level in STZ-induced MIN6 cells. In addition, the AE-administered group lowered blood glucose, increased insulin secretion, and alleviated weight loss in the diabetic rats. Histopathologically, the AE-administered group reduced pancreatic injury by significantly restoring the insulin content in ß-islets. It was observed that the anti-diabetic effects of AE were associated with the suppressed the p38 MAPK pathway and actived the Nrf2 pathway. CONCLUSIONS: The ameliorative impact of AE on diabetes may be attributed to protection of the function of pancreatic ß islets and by improving serum insulin levels, hence reducing the blood glucose, which involved in the p38 MAPK and Nrf2 pathways.

Dietary Ginsenoside T19 Supplementation Regulates Glucose and Lipid Metabolism via AMPK and PI3K Pathways and Its Effect on Intestinal Microbiota.

Ginseng, as a functional food, is widely used worldwide because of its multifarious benefits. Studies have verified that 25-hydroxyl-protopanaxatriol (T19) is a new ginsenoside from ginseng, which had an important inhibitory effect on α-glucosidase and protein tyrosine phosphatase 1B in vitro. This study aims to assess the regulation of T19 against glycolipid metabolism by insulin-resistant HepG2 cells and diabetes mice induced with high-fat diet combined with streptozotocin (STZ). T19 effectively lowered the levels of blood glucose and lipid, alleviated insulin resistance, and improved histological pathology of liver and pancreas. Further study demonstrated that regulation of AMP-activated protein kinase- and phosphoinositide-3-kinase-signaling pathways was involved in the potential mechanism of T19 efficiency. Simultaneously, high-throughput sequencing of 16S rDNA revealed that T19 remarkably ameliorated the high-fat diet/STZ-induced disorders of intestinal microbiota by decreasing the value of Firmicutes/Bacteroidetes, and remarkably raised the relative abundance of the Lachnospiraceae family, which are the beneficial bacteria that can regulate glucose and lipid metabolism. The results may provide clues for further understanding the mechanism of T19 in regulating glycolipid metabolism, and may provide a scientific basis for ginseng as a potential dietary food to prevent metabolic diseases.