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1.
Avicenna J Phytomed ; 11(2): 168-179, 2021.
Article in English | MEDLINE | ID: mdl-33907675

ABSTRACT

OBJECTIVE: The extract of Pinus eldarica bark contains many polyphenolic compounds that were studied due to their high antioxidant, anti-inflammatory and anti-mutagenic effects. Therefore, the purpose of the present study was to conduct phytochemical standardization and develop hard gelatin capsules from the extract of P. eldarica bark. MATERIALS AND METHODS: Extraction was carried out by maceration method at room temperature for 72 hr using ethanol 70% followed by freeze drying. Quantification and standardization tests were performed using Folin-Ciocalteu method. Then, nine formulations were prepared containing different amounts of stearic acid (1-3%) and corn starch (3%, 10%, and 25%). Each formulation was characterized by FTIR and pharmacopoeial tests such as drug content, disintegration time, flowability parameters and drug release percent. The optimized formulation underwent stability studies at 75±5% humidity and 40±2°C. RESULTS: The total phenolic content of the extract in terms of gallic acid equivalent was 362.8±5.4 mg/g and the total procyanidin content in the extract was 174.386±2.5 mg/g. FTIR revealed no interaction between the components. The results presented that the best formulation of the capsules was achieved they contained 3% of stearic acid and 25% of corn starch. This formulation showed 91.69±0.33% of drug content, 9.36±0.02 min disintegration time and 83.02±0.81% release percent. Moreover, it showed good flowability. Stability studies on the optimized formulation displayed that the formulation was stable within 6 months in the accelerated condition. CONCLUSION: In conclusion, results of the present phytopharmaceutical evaluations confirmed this product as a promising herbal capsule formulation.

2.
Cell Biochem Funct ; 37(3): 148-152, 2019 Apr.
Article in English | MEDLINE | ID: mdl-30908696

ABSTRACT

Adiponectin (APN) is an adipocytokine, secreted from adipose tissue and has anti-inflammatory, anti-ageing, and antidiabetic properties. Hyperglycaemia can damage the renal cells, and mammalian target of rapamycin (mTOR), along with Sirtuin 1 (SIRT1), have an important role in kidney cell response to hyperglycaemia. Therefore, understanding the relationship between adiponectin, mTOR, and SIRT1 proteins is beneficial for deciphering the mechanism of adiponectin function. In this study, Human Embryonic Kidney-293 (HEK-293) cells were cultured under normal and high-glucose condition, with and without APN (1, 10, and 100 ng/mL) for 48 hours. mTOR protein expression was evaluated by western blot analysis, and SIRT1 protein was assessed using ELISA method. To evaluate hyperglycaemia-mediated cytotoxicity, cell viability was determined using MTT assay. Data showed that APN in high dose (100 ng/mL) significantly reduced the expression of mTOR and p-mTOR, increased SIRT1 protein, and also improved cell viability compared with the control high glucose (p ≤ 0.05). According to this results, APN can be useful in preventing renal cell damage, by affecting on the expression of mTOR and SIRT1 proteins, as well as increasing the survival of kidney cells in hyperglycaemia conditions. SIGNIFICANCE OF THE STUDY: Adiponectin triggered mTOR/p-mTOR/SIRT1 pathway and decreased cell death in human kidney cells. Our findings provide preliminary experimental data that support further studies on the potential therapeutic role of adiponectin in diabetes and diabetic-induced metabolic complications.


Subject(s)
Adiponectin/pharmacology , Adiponectin/therapeutic use , Hyperglycemia/complications , Kidney Diseases/drug therapy , Kidney Diseases/prevention & control , Cell Survival/drug effects , Cells, Cultured , HEK293 Cells , Humans , Hyperglycemia/drug therapy , Hyperglycemia/pathology , Hyperglycemia/prevention & control , Kidney Diseases/pathology , Sirtuin 1/analysis , Sirtuin 1/antagonists & inhibitors , Sirtuin 1/metabolism , TOR Serine-Threonine Kinases/analysis , TOR Serine-Threonine Kinases/antagonists & inhibitors , TOR Serine-Threonine Kinases/metabolism
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