Introduction: Recently, there has been a significant focus on developing extended-release tablets that regulate drug release at a predetermined rate to maintain optimal therapeutic plasma concentrations. Extended-release formulations offer several clinical advantages, including reducing the frequency of drug administration, minimizing fluctuations in plasma drug concentrations, decreasing adverse effects, and improving therapeutic outcomes.
According to Mongolia’s national pharmaceutical policy, it is essential to conduct quality assurance and safety monitoring studies on imported substitute products included in the national essential medicines list. The policy also mandates the quality control of pharmaceuticals in internationally accredited laboratories compliant with MNS ISO/ IEC 17025:2018 standards. Methods: The quality control parameters of Diclofenac Sodium Retard 100 mg tablets from three different manufacturers were evaluated by the methodologies outlined in the United States Pharmacopeia USP32 and USP44. The study assessed physical appearance, average weight, weight variation, friability, dissolution, and quantitative drug content determination. Results: The average weight and weight variation of Diclofenac Sodium Retard 100 mg tablets from three different manufacturers were as follows: Tablet A: (+3.60%, -2.84%), Tablet B: (+1.53%,-1.86%), Tablet C: (+2.53%,-1.96%). The friability and mechanical strength tests determined that all three tablets exhibited 99.9% friability resistance. The quantitative determination of Diclofenac Sodium content per tablet was: Tablet A: 0.098 g, Tablet B: 0.105 g, Tablet C: 0.104 g. Microbiological purity analysis showed that in all three tablets (A, B, and C), The total aerobic bacterial count was <101 CFU. The total mold and yeast count was <101 CFU and Escherichia coli was not detected. Dissolution test results showed the following percentage of drug released at different time points: Tablet A: 60 min: 16.1%, 120 min: 24.7%, 240 min: 39.6%, 360 min: 52.3%, 600 min: 73.6%. Tablet B: 60 min: 18.4%, 120 min: 26.1%, 240 min: 39.1%, 360 min: 55.8%, 600 min: 75.2%. Tablet C: 60 min: 18.6%, 120 min: 31.4%, 240 min: 52.9%, 360 min: 65.9%, 600 min: 77.0%. These results demonstrate that all tested tablets met the dissolution requirements of USP 44, 2021. Conclusion The findings indicate that the three manufacturers’ Diclofenac Sodium Retard 100 mg tablets comply with the quality standards set by the United States Pharmacopeia (USP 32 and USP 44) and Mongolian Pharmacopoeia 2011.

The process of ALI is associated with excessive pulmonary inflammation as undue activation of immune cells including macrophages and neutrophile granulocytes and subsequently increased cytokines such as interleukin 6 (IL-6) contribute to severe tissue damage and irreversible pulmonary pathological changes. NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome is a cytosolic receptor consisting of upstream sensor protein NLRP3, adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC) and the effector protein caspase-1. Nuclear factor E2-related factor 2 (Nrf2) is a transcription factor that neutralizes oxidative stress via initiating antioxidant response element-driven gene transcription. Nrf2 is suppressed by kelch-like ECH-associated protein 1 (Keap1) under physiological conditions, while Nrf2 dissociates from Keap1, stabilizes and accumulates in the nucleus with stimulation of oxidative stress. Thereafter, heme oxygenase 1 (HO-1) a downstream target gene of Nrf2 is activated to catalyze various detoxification reactions and exert anti-oxidative capacity.
ISO significantly promoted the expression of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and down-regulated kelch-like ECH-associated protein 1 (Keap1). Simultaneously, it suppressed the over-expression of NOD-, LRR- and pyrin domain-containing 3 (NLRP3), caspase-1, apoptosis-associated speck-like protein containing a CARD (ASC) and pro-inflammatory cytokines interleukin IL-1β (pro-IL-1β), and inhibited the expression of apoptotic related proteins induced by LPS challenge. Meanwhile, the results of molecular docking indicated the potential ability of ISO as a ligand binding with proteins Keap1, NLRP3 and cleaved-caspase-3 as well.

Introduction: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) usually result in significant mortality and are featured by pulmonary edema, dysregulated inflammation, and alveolar/capillary barrier destruction. ALI is derived from various lung injuries such as severe pulmonary infection, near drowning, lung contusion, and pulmonary embolism. Methods: This research work was supported by the National Natural Science Foundation of China, Natural Science Foundation of Jiangsu Province. LPS (from Escherichia coli O55:B5) was purchased from Sigma (St. Louis, MO, USA). Dexamethasone (DEX) was supplied by Shenyang Guangda Pharmaceutical Co., Ltd. The SOD, NO, MPO, and IL-6 assay kits were obtained from Nanjing Jiancheng Bioengineering Institute (Nanjing, China). The identification was performed by Professor Tserendulam Luvsandorj at the Mongolian University of Pharmaceutical Science and specimens were preserved in the School of Traditional Chinese Pharmacy, China Pharmaceutical University. TML was soaked with water for 30 min and decoction three times was conducted with the solid-liquid ratio of 1:10, 1:8, and 1:6, respectively. ICR male mice (8 weeks old, 22–25 g) were purchased from Henan Sikes’s Biotechnology Co., Ltd (Henan, China). Statistical tests were performed using IBM SPSS Statistics version 26.0 Software (SPSS, Inc., Chicago, IL, USA) and presented as mean ± standard deviation for continuous variables. Conclusion In summary, the effect of TML on acute lung injury has been studied with Isoorientin, one of its biologically active compounds. Studies have demonstrated that Isoorientin has been shown to protect against pulmonary edema, inflammatory cells, and inflammatory cytokine mediator expression in acute lung injury caused by LPS. Therefore, we have a certain need to study the mechanisms by which this protective effect takes place further.