Diabetes is a chronic disease caused by metabolic disorders due to abnormal blood glucose levels, and insulin is a commonly used drug in the treatment of diabetes. Different types of insulin exhibit different clinical efficacy due to their mechanisms and duration of action in the body, the basal long-acting release and postprandial controlled release of insulin have always been hot topics among clinical researchers. With the development of nanotechnology, the research and development of new nano-drug carriers with excellent drug release properties have become an important opportunity to solve clinical targeted medication, especially the loading of insulin by metal-based nanocarriers is expected to be an effective path to enhance the therapeutic efficacy in clinical diabetic patients. Herein, around the controllable release of insulin, the basic categories and characteristics of clinical insulin are briefly introduced, and the synthesis of metal-based nanocarriers and their drug release performance for insulin are emphasized. The performance of gold-based, iron-based, copper-based, and zinc-based metal-based nanocarriers in insulin loading are analyzed, the characteristics of different metal-based nanocarriers in insulin loading are introduced through specific comparative parameter, the mechanism and typical features of insulin loading elaborated by metal-based nanocarriers, and the influencing factors of carrier size, carrier morphology, and surface functionalization on the insulin release from carriers are also discussed. Finally, reflects on existing issues and provides insights into future directions, aiming to offer technical references and new ideas for the treatment of clinical diabetes.

With the rapid development of contemporary medical technology, long-acting in situ forming preparations have emerged as a pivotal area of investigation in the field of drug delivery. Owing to its unique drug release characteristics, sustained therapeutic effect, enhanced dosing precision and other notable benefits, it represents a transformative approach for clinical treatment. In this study, an in-depth analysis of the characteristics of different technology platforms, the critical technical challenges in the process of industrialization and the emerging trends was conducted through a comprehensive review of products approved by FDA, EMA and other regulatory authorities and the research pipelines global and domestic. The findings aim to provide a strategic framework to support the industrialization of long-acting preparations in China.

Acne vulgaris is a chronic inflammatory skin disease, mainly caused by clogged and inflamed hair follicles, and is the eighth most common disease worldwide, severely affecting people's quality of life. Although several treatment options are available, such as pharmacotherapy and physiotherapy, most medications suffer from significant side effects, poor chemical stability, and low targeting efficacy. Drug delivery systems (DDS) have potential applications in acne treatment, particularly in enhancing drug efficacy and minimizing side effects. Therefore, the development of novel DDS has become the focus of current research. This review firstly analyzes the pathological mechanisms of acne vulgaris and its therapeutic targets, secondly systematically outlines the existing therapeutic approaches, and finally focuses on the potential applications of DDS in acne treatment, aiming to provide new perspectives and options for future acne treatment.

As one of the classic Chinese herbs, spore powder has a long history of medicinal value, not only in terms of therapeutic efficacy, but also through the defatting and removal of the contents can be constructed sporopollenin (SP) cavity structure, which can be used as a highly efficient drug carrier. Compared with synthetic carriers, sporopollenin, as a natural biomaterial, has demonstrated multiple applications in biomedical fields by virtue of its excellent biocompatibility, physicochemical stability, and dimensional homogeneity, and has successfully achieved efficient loading of anti-tumour drugs, proteins, and other active ingredients, and can be further developed into a smart drug delivery system by surface modification technology. In this paper, we summarise the preparation process, loading mechanism, drug delivery system design principle of sporopollenin from traditional Chinese medicine, and its research progress on intelligent drug delivery system, such as targeted delivery and responsive release, and discuss its development prospect, with a view to providing theoretical references and technological support for the promotion of the wide application of traditional Chinese medicine-derived sporopollenin microcapsules in the field of biomedicine.

Artificial intelligence (AI) has progressively integrated into various fields and plays a significant role. With the advent of China's aging population era and the growing public demand for healthcare, the application of AI in the field of clinical pharmacy has garnered considerable attention. Clinical pharmacy is crucial for ensuring the safety and effectiveness of clinical medication use by optimizing drug therapy and preventing medication errors. Due to its advantages, such as powerful data processing and analysis capabilities, and robust model-based predictive abilities, AI holds broad application prospects in the field of clinical pharmacy. This article introduces the current progress in AI applications within clinical pharmacy, focusing on its use in enhancing drug efficacy and safety. These applications include: assisting drug selection, optimizing dosage and administration timing, providing intelligent pharmaceutical services, predicting drug-drug interactions, pharmacovigilance, and preventing medication errors. Building on a review of current advancements, the article also discusses the challenges faced in implementing these AI applications. It proposes potential solutions, aiming to provide a reference for subsequent research and relevant practitioners.

This study aimed to investigate the inhibitory effects of Hua Chan Su (HCS) on non-small cell lung cancer (NSCLC) both in vitro and in vivo, and to elucidate the molecular mechanism by which it induces endoplasmic reticulum (ER) stress. Firstly, using the CCK-8 assay to assess the proliferation of human lung adenocarcinoma A549 cells, it was found that HCS significantly inhibited cell proliferation and reduced migratory capacity. Transcriptome sequencing revealed that HCS down-regulated anti-apoptotic genes such as B-cell lymphoma-2 (Bcl2) and was enriched in signaling pathways related to the cell cycle, apoptosis, and ER stress. Further studies demonstrated that HCS enhanced mitochondrial oxidative stress, increased the expression of Bcl2 associated X, decreased the expression of Bcl2, and induced apoptosis. Western blot analysis showed that HCS significantly activated the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor 2α (eIF2α)- activating transcription factor 4 (ATF4) signaling pathway in vitro. Combined with a PERK inhibitor, it was confirmed that HCS could trigger apoptosis through the ER stress pathway. In animal experiments, oral administration of HCS (2 and 4 g·kg^-1) for 14 consecutive days significantly inhibited the growth of NSCLC xenografts, with no observed toxicity in major organs. TUNEL staining and Western blot analysis further confirmed that HCS induced tumor cell apoptosis in vivo (all animal experiments were approved by the Institutional Animal Ethics Committee of Nanjing University of Chinese Medicine, approval number: ACU240307). Serum biochemical results suggested that HCS improved liver function and oxidative stress status. In addition, immunohistochemical analysis showed that HCS down-regulated mesenchymal markers such as vimentin, α-smooth muscle actin (α-SMA), and fibroblast activation protein 1 (FAP1), while up-regulating E-cadherin levels, significantly inhibiting the epithelial mesenchymal transition (EMT) process in NSCLC cells. In conclusion, HCS can activate the PERK-eIF2α-ATF4 signaling pathway to induce tumor cell apoptosis and inhibit EMT, indicating its potential application value in the treatment of non-small cell lung cancer.

Objective to study the efficacy and mechanism of Renzhu Jianwei Granules in treating chronic atrophic gastritis (CAG) with the precancerous lesions of gastric cancer, CAG rat models were induced using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) comprehensive factor modeling method. After successful modeling, Renzhu Jianwei Granules were administered by gavage. Evaluating the efficacy of Renzhu Jianwei Granules by observing their effects on gastric acid pH, food intake, body weight, serum levels of pepsinogen (PG), gastrin (GAS), motilin (MTL), and inflammatory factors TNF-α, IL-1α, and IL-6 in CAG rats; Hematoxylin-Eosin (H&E) staining and Alcian blue-periodic acid Schiff (AB-PAS) staining were used to observe pathological changes in the gastric antral tissue; TUNEL fluorescence staining was used to observe apoptosis of gastric mucosal epithelial cells; immunofluorescence staining was used to detect the expression of PCNA and p53 proteins in the gastric mucosa; qRT-PCR was used to detect the mRNA expression of p53, Mdm2, Bcl-2, Bax, and Tnf-α, Il-1α, Il-6 in gastric tissue; Western blot was used to detect the protein expression of PTEN, Akt, NF-κB, p53, MDM2, Bcl-2, Bax in gastric tissue, and immunofluorescence staining technology was used to detect the protein expression of Bcl-2/Bax in gastric tissue. Animal experiments approved by the Ethics Committee of China Pharmaceutical University (approval No. 2022-09-029). The results show Renzhu Jianwei Granules significantly reduced the gastric acid pH in rats, increased food intake and body weight, and decreased the serum levels of PGI/PGⅡ, GAS, MTL, TNF-α, IL-1α, IL-6 (P < 0.01); increased the mRNA expression levels of p53, Bax in the gastric antral tissue (P < 0.05, P < 0.01), and decreased the mRNA expression levels of Mdm2, Bcl-2, Tnf-α, Il-1α, Il-6 in the gastric tissue (P < 0.01); significantly increased the protein expression levels of PTEN, p53, Bax in the gastric tissue (P < 0.05, P < 0.01), and downregulated the expression of p-NF-κB, p-Akt, MDM2, Bcl-2 proteins (P < 0.05, P < 0.01). To sum up, Renzhu Jianwei Granules treat CAG by intervening in the PTEN/Akt/p53 pathway, inducing cell apoptosis, and preventing precancerous lesions.

Cell-penetrating peptides (CPPs), such as TAT and L17E, have demonstrated significant potential in drug delivery, particularly in protein delivery. Previous studies have shown that TAT fusion proteins exhibit superior delivery efficiency compared to non-fusion counterparts and under non-covalent conjugation conditions, L17E demonstrates superior delivery efficiency compared to TAT in transporting EGFP into cells. Therefore, this study investigates the ability of TAT and L17E to deliver target proteins via covalent fusion strategies, along with their molecular-level mechanisms of action. The fusion proteins TAT-EGFP and L17E-EGFP were expressed and purified. They were evaluated for their abilities to penetrate B16-F10 cells using flow cytometry and fluorescence microscopy. The results revealed that TAT-EGFP exhibited stronger membrane-penetrating ability, with delivery efficiency positively correlated with fusion protein concentration. Structural simulations using AlphaFold3 indicated that TAT-EGFP possesses two outward-extending hydrophobic side chains, a structural feature likely enhancing its interaction with the cell membrane and thereby improving penetration efficiency. In contrast, L17E-EGFP displayed inward-retracted side chains and intramolecular electrostatic interactions, which may reduce binding sites and contact area with the cell membrane, impairing penetration efficacy. This study demonstrates that the structural characteristics of cationic cell-penetrating peptides, such as TAT and L17E (including side chain conformation, hydrophobicity, and charge distribution) are critical determinants of their delivery efficiency, providing a pivotal foundation for optimizing CPP design and advancing CPP-mediated protein drug development.

This study is based on the "indirect regulation" strategy to explore the effects of astragaloside Ⅳ (AG) and its analogs cycloastragenol (CAG) and astragenol (HG) in regulating the gut microbiota to improve Parkinson's disease (PD). Through the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced PD mouse model, combined with behavioral experiments, immunofluorescence staining, Western blot, and 16S rRNA sequencing, the therapeutic effects and potential mechanisms of the three compounds were systematically evaluated (the animal experiment was approved by the Animal Medical Ethics Committee of Shanxi University of Chinese Medicine, the approval number is AWE202307367). The results showed that AG, CAG, and HG (30 mg·kg^-1) could significantly improve the behavioral phenotypes such as gait abnormalities and bradykinesia in PD mice, and restore the number of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra region, and inhibit the expression of ionized calcium binding adapter molecule 1 (Iba-1), a marker of microglial cell activation. Among them, CAG had the best effect among the three, which was comparable to that of the positive drug levodopa (70 mg·kg^-1). The analysis of the gut microbiota indicated that all three compounds could reverse the decrease in microbiota diversity induced by MPTP and adjust the abundances of PD disease-related genera Akkermansia, Lactobacillus, and Ruminococcus. AG specifically promoted the enrichment of the genus Allobaculum, while CAG and HG significantly increased the abundance of the genus Blautia, suggesting that they inhibited neuroinflammation by regulating microbiota metabolites (such as short-chain fatty acids). The study demonstrates that AG, CAG, and HG can indirectly regulate the structure of the gut microbiota through the "gut-brain axis" and inhibit central neuroinflammation, thus improving the pathological process of PD. This provides a multi-target intervention strategy based on natural products for the treatment of PD.

Previous investigations have established that ferulic acid demonstrates anti-fibrosis effects and could inhibit the activation of hepatic stellate cell. Injury, proliferation and capillarization of hepatic sinusoidal endothelial cell are important forms of angiogenesis during liver fibrosis, and is important for liver fibrosis regression. This study investigates the effects of ferulic acid on sinusoidal capillarization and explores its anti-fibrotic mechanism. In vitro, SK-HEP-1 cells were injured by cobalt chloride, while human hepatic sinusoidal endothelial cells (HHSECs) were induced by endothelial cell growth supplement (ECGs). Cell viability was detected using thiazolyl blue tetrazolium bromide (MTT); nitric oxide (NO) and nitric oxide synthase (NOS) were visualized through the fluorescence probe method; antiangiogenesis effects were assessed using the tube formation assay and transgenic zebrafish (VEGFR: GFP). Animal experiments complied with the regulations of the Animal Ethics Committee of Shanghai University of Traditional Chinese Medicine (approval No. PZSHUTCM2503280008). Mice were received intraperitoneal injection of carbon tetrachloride (CCl₄) for 6 weeks to induce hepatic fibrosis and then treated with 10 mg·kg^-1 of sorafenib, 50 and 100 mg·kg^-1 of ferulic acid for 3 weeks from the fourth week. Liver inflammation and fibrosis were assessed through serum liver function [alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB)] tests, H & E and Sirius red staining, hydroxyproline (HYP) quantification, and the immumohistochemical staining of α-smooth muscle actin (α-SMA). Sinusoidal fenestrations were observed via scanning electron microscopy (SEM), and the phenotype of liver sinusoidal endothelial cells were labeled by platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE1). Results showed that ferulic acid protected SK-HEP-1 cells from CoCl₂-induced hypoxic injury, significantly increased NO and NOS levels. It suppressed the proliferation and tube formation of HHSEC, and inhibited angiogenesis of VEGFR: GFP zebrafish model. In vivo experiments, ferulic acid reduced serum AST/ALT and HYP levels and increased ALB. Histopathological analyses confirmed that it reduced inflammation and fibrosis, downregulated α-SMA expression, ameliorated sinusoid capillarization and downregulated the expression of CD31 and LYVE1. These findings indicate that ferulic acid can inhibit liver fibrosis through alleviating sinusoidal capillarization.