Synacinn™, a standardized polyherbal supplement, was shown to improve hyperglycemic conditions and related complications in STZ-induced rats.
Curcumin was found to be an active constituent that might contribute to the inhibition of SynacinnTM against CYP2C8, CYP2C9 and CYP2C19. It can be suggested that SynacinnTM can be consumed separately from a drug known to be metabolized by all tested CYP450 enzymes.
A HPLC method has been validated for identifying five markers (gallic acid, rosmarinic acid, catechin, andrographolide and curcumin) and quantifying curcumin in Synacinn TM formulation. The validation (bracketed strengths of 10 mg/mL and 100 mg/mL) involved assessment of selectivity, precision, Limit of Detection (LOD), Limit of Quantification (LOQ), linearity, accuracy, stability in diluent and formulation stability. Meanwhile, in vivo bone marrow micronucleus test data was presented to evaluate the toxicity potential of Synacinn™ to cause clastogenicity and/or disruption of the mitotic apparatus, as measured by its ability to induce micronucleated polychromatic erythrocytes (MN PCE) in Sprague Dawley rat bone marrow. The test was conducted in two phases viz., Phase I (Dose Range Finding experiment) and Phase II (Definitive experiment). Phase I was conducted to assess general toxicity and bone marrow cytotoxicity of Synacinn™, and to select the doses for the definitive experiment. In-life observations included mortality, clinical signs of toxicity and body weight. Bone marrow samples were collected and extracted from the femur bone using fetal bovine serum. The pellet obtained after the centrifugation was used for preparing bone marrow smears to evaluate the number of immature and mature erythrocytes.
The present data described the analysis of mutagenicity in Synacinn TM by assessing the point mutations occurring due to Synacinn™ exposure to five tester strains of Salmonella typhimurium (TA1537, TA1535, TA98, TA100 and TA102), in the presence or absence of an exogenous mammalian metabolic activation system (S9). It was conducted in two Phases - Phase I (Dose Range Finding experiment-DRF) and Phase II (Mutagenicity Assay 1 and 2). DRF and Mutagenicity Assay 1 was conducted employing plate incorporation method, while Mutagenicity Assay 2 was performed using pre-incubation method. Formulation analysis pertaining to Synacinn TM was performed for both Mutagenicity Assay 1 and 2. Dose formulations were prepared fresh on each day of the experiment. Adventol 50% v/v in purified water was selected as a suitable vehicle based on the preliminary solubility test. Based on the Phase I analysis, 5 mg/plate was selected as the highest concentration of Synacinn TM followed by lower concentrations of 2.5, 1.25, 0.625 and 0.313 mg/plate for the Mutagenicity Assays. Genetic integrity of all the tester strains used was confirmed by performing genotyping before their use. All the data acceptability criteria were fulfilled confirming the validity of the test.
Synacinn is a standardized polyherbal extract formulated for the treatment of diabetes mellitus and its complications. This study aims to assess the mutagenicity potential of Synacinn by Ames assay and in vivo bone marrow micronucleus (MN) test on Sprague Dawley rat. Human ether-a-go-go-related gene (hERG) assay and Functional Observation Battery (FOB) were done for the safety pharmacology tests. In the Ames assay, Dose Range Finding (DRF) study and mutagenicity assays (+/− S9) were carried out. For the MN test, a preliminary and definitive study were conducted. In-life observations and number of immature and mature erythrocytes in the bone marrow cells were recorded. The hERG assay was conducted to determine the inhibitory effect on hERG potassium channel current expressed in human embryonic kidney cells (HEK293). FOB tests were performed orally (250, 750, and 2000 mg/kg) on Sprague Dawley rats. Synacinn is non-mutagenic against all tested strains of Salmonella typhimurium and did not induce any clastogenicity in the rat bone marrow. Synacinn also did not produce any significant inhibition (p ≤ 0.05) on hERG potassium current. Synacinn did not cause any neurobehavioural changes in rats up to 2000 mg/kg. Thus, no mutagenicity, cardiotoxicity and neurotoxicity effects of Synacinn were observed in this study.
R-38TM is a traditional herbal supplement for treating arthritis-related conditions. High-performance liquid chromatography (HPLC) analysis was performed for identification and quantification of rosmarinic acid in the R-38TM water extract. The anti-arthritic potential of the R-38TM water extract was investigated by measuring the production of IL-6 and TNF-α in inflamed cells. Xanthine oxidase (XO) and cyclooxygenase-2 (COX-2) inhibition assays were also conducted. The cytotoxic effect of R-38TM water extract was investigated on HSF1184 cell line. Acute and subacute oral toxicity studies were conducted on female Sprague-Dawley (SD) rats. The rosmarinic acid was identified at 1.208 min (3.61 %w/w). The inflamed cells showed a decrease in the production of IL-6 (55.9%) and TNF-α (52.13%). The COX-2 and XO enzymes were moderately inhibited by R-38TM water extract. The cytotoxicity analysis showed no cytotoxic effect on the cell. The acute and subacute oral toxicity studies revealed no mortality and normal body weight at all doses. There were no significant differences (p > 0.05) in organ weight, hematological and biochemical parameters, and histology of liver and kidneys with the control group. In conclusion, R-38TM water extract exhibited no toxic effect orally and may possess potential therapeutic properties against pro-inflammatory diseases including arthritis.
In this study, Syzygium polyanthum was standardized against gallic acid (GA), and a complete pharmacokinetic test was conducted using in vitro and in vivo models against this phytochemical. High-performance liquid chromatography showed that GA is a major phytochemical in aqueous extract of S. polyanthum. It exhibited a low equilibrium solubility and physiochemical stability at pH 2.0 and 7.4, but it deteriorated rapidly at pH 9.2. It showed low permeability toward Caco-2 intestinal absorption with eight times slower absorption in oral than intravenous administration. GA was unstable in mouse, rat, and dog plasma sera with in vitro half-lives (t1/2) of 60, 53, and 56 min, respectively, but was relatively stable in human plasma serum (t1/2 = 185 min). Approximately 5.6% of GA (10 µM) bound to the human plasma proteins. GA was stable in mouse, rat, dog, and human microsomal extracts with in vitro microsomal intrinsic clearance values of 72, 68, 6, and 22 µL/min/mg, respectively. GA selectively inhibited or stimulated the activity of the tested CYP450 enzymes. The in vivo oral bioavailability of GA was 54%, with short elimination half-life and a high volume of distribution. Thus, the mention pharmacokinetic features of GA must be considered during the development of GA-based products to yield the optimum dosage and pharmacological effect.
INTRODUCTION: The study aimed to assess the safety and nutraceutical properties of ALLURATM related to women’s health and skin beautification. MATERIALS AND METHODS: Determinations of total phenolic (TPC) and flavonoid contents (TFC) were done using the colorimetric method, followed by the identification of gallic acid via highperformance liquid chromatography (HPLC). Antioxidant activity was analyzed using 2,2 -diphenyl-2-picrylhydrazyl (DPPH) and 2,2’-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid (ABTS) radicals while its anti-inflammatory activity was measured using enzymelinked immunosorbent assay (ELISA). Anti-aging and whitening effects were determined by porcine elastase and mushroom tyrosinase activities, respectively. Skin cell growth promotion and rejuvenation were evaluated using in vitro scratch assay. Cytotoxicity assay was done using HSF1184 and 3T3 BALB/c cell lines. While, acute toxicity test was done on two groups (control and treatment) of six Wistar rats each. The nutraceutical properties were evaluated based on proximate analysis. RESULTS: ALLURATM exhibited DPPH-IC50 values of 180.40 µg/mL and ABTS-IC50 value of 174.40 µg/mL. TPC and TFC were 67.31 mg GAE/g extract and 43.21 mg CE/g extract, respectively while 10.98 mg/g of gallic acid were quantified. ALLURATM reduced pro-inflammatory cytokines of TNF-α and IL-6 and showed anti-aging (IC50-162.40 µg/mL) and whitening effects (IC50- 167.70 µg/mL). ALLURA™ also increased the proliferation of HSF1184 (≤ 1000 µg/ mL), producing significant secretion of epidermal growth factor (EGF) and shown to be non-cytotoxic. No mortality was observed at the highest dose of 2000 mg/kg b.w.t. nor the behavioral and morphological changes in rats. The proximate analysis resulted in high content of moisture and low calories. CONCLUSION: These findings provided preliminary reports for the first time on the functionality of ALLURA™ for its anti-inflammatory, antioxidant, and nutraceutical properties.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.