Bergenia pacumbis from Nepal, an astonishing enzymes inhibitor.

BACKGROUND: The Bergenia species are perennial herbs native to central Asia, and one of the most promising medicinal plants of the family Saxifragaceae which are popularly known as 'Pashanbheda'. The aim of this study was to evaluate antioxidant and α-amylase, α-glucosidase, lipase, tyrosinase, elastase, and cholinesterases inhibition potential of Bergenia pacumbis of Nepali origin collected from the Karnali region of Nepal. METHODS: The sequential crude extracts were made in hexane, ethyl acetate, methanol, and water. Antioxidant activities were analyzed by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assay. The α-amylase, α-glucosidase, lipase, tyrosinase, elastase, acetylcholinesterase, and butyrylcholinesterase inhibition were analyzed by the 3,5-Dinitrosalicylic acid (DNSA), p-Nitrophenyl-α-D-glucopyranoside (p-NPG), 4-nitrophenyl butyrate (p-NPB), l-3,4-dihydroxyphenylalanine (L-DOPA), N-Succinyl-Ala-Ala-p-nitroanilide (AAAPVN), acetylthiocholine, and butyrylcholine as a respective substrate. The major metabolites were identified by high performance liquid chromatography with electron spray ionization- quadrupole time-of-flight mass spectrometry (HPLC-ESI-QTOF-MS) profiling. RESULTS: Our results revealed the great antioxidant ability of crude extract of B. pacumbis in ethyl acetate extract against both DPPH (IC50 = 30.14 ± 0.14 µg/mL) and ABTS (IC50 = 17.38 ± 1.12 µg/mL). However, the crude methanol extract of B. pacumbis showed the comparable enzymes inhibitions with standard drugs; α-amylase (IC50 = 14.03 ± 0.04 µg/mL), α-glucosidase (IC50 = 0.29 ± 0.00 µg/mL), lipase (IC50 = 67.26 ± 0.17 µg/mL), tyrosinase (IC50 = 58.25 ± 1.63 µg/mL), elastase (IC50 = 74.00 ± 3.03 µg/mL), acetylcholinesterase (IC50 = 31.52 ± 0.58 µg/mL), and butyrylcholinesterase (IC50 = 11.69 ± 0.14 µg/mL). On the basis of HPLC-ESI-QTOF-MS profiling of metabolites, we identified major compounds such as Bergenin, Catechin, Arbutin, Gallic acid, Protocatechuic acid, Syringic acid, Hyperoside, Afzelechin, Methyl gallate, Paashaanolactone, Astilbin, Quercetin, Kaempferol-7-O-glucoside, Diosmetin, Phloretin, and Morin in methanol extract which has reported beneficial bioactivities. CONCLUSION: Our study provides a plethora of scientific evidence that the crude extracts of B. pacumbis from Nepalese origin in different extracting solvents have shown significant potential on inhibiting free radicals as well as enzymes involved in digestion, skin related problems, and neurological disorders compared with the commercially available drugs.

Abresham ameliorates dyslipidemia, hepatic steatosis and hypertension in high-fat diet fed rats by repressing oxidative stress, TNF-α and normalizing NO production.

This study was aimed to investigate whether standardized hydroalcoholic extract of abresham (AB) ameliorates dyslipidemia, hepatic steatosis and associated hypertension in rats fed with high-cholesterol/high-fat diet (HFD). HFD (55% calorie from fat and 2% cholesterol) were fed for 45 days to induce dyslipidemia, hepatic steatosis and associated hypertension. After confirmation of hypercholesterolemia (total cholesterol >150 mg/dl) on 30th day, different doses of AB (200-800 mg/kg/day) were administered for next 15 days. HFD administration for 45 days led to cardiometabolic syndrome characterized by significant increase in body weight, total cholesterol, triglyceride, low density lipoprotein cholesterol, TNF-α levels along with decrease in high density lipoprotein cholesterol and serum NO level. Furthermore, HFD resulted in significant increase in systolic arterial pressure, diastolic arterial pressure and mean arterial pressure. In addition, morphological studies revealed hepatic steatosis along with swelling of mitochondria and loss of cristae in hepatocyte and periarteritis in aorta. Treatment with AB for 15 days positively modulated the altered parameters in dose-dependent fashion, though maximum effect was seen at 800 mg/kg. These findings suggest that AB guard against cardiometabolic syndrome in HFD fed rats. It attenuates dyslipidemia, hepatic steatosis and associated hypertension by decreasing oxidative stress, TNF-α and normalizing NO production.

Upregulation of PPARγ by Aegle marmelos ameliorates insulin resistance and ß-cell dysfunction in high fat diet fed-streptozotocin induced type 2 diabetic rats.

The global epidemic of type 2 diabetes demands the rapid evaluation of new and accessible interventions. This study investigated whether Aegle marmelos fruit aqueous extract (AMF; 250, 500 and 1000 mg/kg) improves insulin resistance, dyslipidemia and ß-cell dysfunction in high fat diet fed-streptozotocin (HFD-STZ)-induced diabetic rats by modulating peroxisome proliferator-activated receptor-γ (PPARγ) expression. The serum levels of glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), homeostasis model assessment of ß-cell function (HOMA-B), lipid profile, TNF-α and IL-6 were evaluated. Further, the TBARS level and SOD activity in pancreatic tissue and PPARγ protein expression in liver were assessed. In addition, histopathological and ultrastructural studies were performed to validate the effect of AMF on ß-cells. The HFD-STZ treated rats showed a significant increase in the serum levels of glucose, insulin, HOMA-IR, TNF-α, IL-6, dyslipidemia with a concomitant decrease in HOMA-B and PPARγ expression. Treatment with AMF for 21 days in diabetic rats positively modulated the altered parameters in a dose-dependent manner. Furthermore, AMF prevented inflammatory changes and ß-cell damage along with a reduction in mitochondrial and endoplasmic reticulum swelling. These findings suggest that the protective effect of AMF in type 2 diabetic rats is due to the preservation of ß-cell function and insulin-sensitivity through increased PPARγ expression.

Effect of Piper betle on cardiac function, marker enzymes, and oxidative stress in isoproterenol-induced cardiotoxicity in rats.

The present study was designed to investigate the cardioprotective potential of Piper betle (P. betle) against isoproterenol (ISP)-induced myocardial infarction in rats. Rats were randomly divided into eight groups viz. control, ISP, P. betle (75, 150, and 300 mg/kg) and P. betle (75, 150, and 300 mg/kg) + ISP treated group. P. betle leaf extract (75, 150, or 300 mg/kg) or saline was orally administered for 30 days. ISP (85 mg/kg, s.c.) was administered at an interval of 24 h on the 28(th) and 29(th) day and on day 30 the functional and biochemical parameters were measured. ISP administration showed a significant decrease in systolic, diastolic, mean arterial pressure (SAP, DAP, MAP), heart rate (HR), contractility (+LVdP/dt), and relaxation (-LVdP/dt) and increased left ventricular end-diastolic pressure (LVEDP). ISP also caused significant decrease in myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and myocyte injury marker enzymes; creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH) along with enhanced lipid peroxidation; thiobarbituric acid reacting species (TBARS) in heart. Pre-treatment with P. betle favorably modulated hemodynamic (SAP, DAP, and MAP) and ventricular function parameters (-LVdP/dt and LVEDP). P. betle pre-treatment also restored SOD, CAT, GSH, and GPx, reduced the leakage of CK-MB isoenzyme and LDH along with decreased lipid peroxidation in the heart. Taken together, the biochemical and functional parameters indicate that P. betle 150 and 300 mg/kg has a significant cardioprotective effect against ISP-induced myocardial infarction. Results of the present study suggest the cardioprotective potential of P. betle.