Comprehensive quantitative and comparative risk data on drug-induced acute kidney injury (AKI) remain limited. Thus, this study aimed to supplement the current data with information from the FDA Adverse Event Reporting System (FAERS) database.

Based on the collected AKI-related reports in the FAERS database from 2004 to 2023, we summarized a list of reported nephrotoxic drugs, compiling counts of the most frequently reported single drugs and drug classes. A disproportionality analysis was used to evaluate the AKI risk of reported drugs, and histological and onset time analyses were conducted.

A total of 1456 drugs were reported as culprit drugs in the 327,561 AKI-related reports in the FAERS database, most of which were antineoplastic agents. Omeprazole was the most frequently reported single drug, followed by furosemide, pantoprazole, esomeprazole, and lansoprazole. Drugs for acid-related disorders were the most commonly reported drug class, followed by agents acting on the renin–angiotensin system, antineoplastic agents, immunosuppressants, and analgesics. In the disproportionality analysis, 1021 drugs showed different degrees of association with the occurrence of AKI, among which eight drugs (spironolactone, mycophenolic acid, enalapril, valsartan, candesartan, gentamicin, vancomycin, and nifedipine) had the largest number of positive signals, with 15 positive signals each. Drugs acting as an antineoplastic agent were the class with the largest number of positive signal drugs in most preferred term groups; however, the imbalance of risk signal distribution among drug classes reflected the subsequent risk differences in relation to AKI. In the histological analysis, tubulointerstitial injury was the most commonly reported type of histological injury. In the onset time analysis, vancomycin presented the shortest median onset time, while the median onset time for lansoprazole was the longest.

Our study integrated quantitative and comparative AKI risk data for 1456 reported culprit drugs using the FAERS database, which can provide reference information for clinical practice.

Periplaneta americana is an important traditional medicine in China. Moreover, Periplaneta americana is effective in treating multiple tumor types. Thus, this study aimed to investigate the combined effects of Periplaneta americana extract CII-3 (an active component from Periplaneta americana) and 5-fluorouracil (5-FU) on liver cancer in mice, focusing on anti-tumor and immunomodulatory properties.

Mice were divided into five groups: normal, model, CII-3, 5-FU and 5-FU+CII-3. Continuous treatment for 14 days included monitoring tumor volume and weight, calculating spleen and thymus indices, and observing tumor tissue morphology. Immunological assays evaluated natural killer (NK) cell cytotoxicity, T/B lymphocyte proliferation, and the proportions of CD3+, CD4+, and CD8+ cells. ELISA was employed to assess serum levels of IgA, IgM, IgG, and interleukin-8 (IL-8). The reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were utilized to analyze the mRNA and protein expressions, respectively, of toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), tumor necrosis factor receptor-associated factor 6 (TRAF6), myeloid differentiation primary response protein 88 (MyD88) and tumor necrosis factor-α (TNF-α) in tumors.

Compared to the 5-FU group, the 5-FU+CII-3 group showed reduced tumor mass and increased spleen and thymus indices. Tumor tissue in the treatment groups exhibited a loose structure, characterized by nuclear fragmentation and the presence of lipid vacuoles. The 5-FU+CII-3 group exhibited enhanced NK cell cytotoxicity, T/B lymphocyte proliferation, CD3+ proportion, CD4+/CD8+ ratio and serum levels of IgA, IgM, and IgG, alongside a reduction in IL-8 content. The levels of TLR4, NF-κB, MyD88, and TNF-α mRNA and protein expressions were downregulated, while TRAF6 mRNA expression was also notably decreased in the tumor tissue.

The CII-3 and 5-FU combined treatment synergistically exerts anti-tumor and immunomodulatory effects, potentially mediated through the regulation of TLR4, NF-κB, TRAF6, MyD88, and TNF-α.

Opioid overdose represents a critical public health issue that has attracted considerable research interest. Therefore, objective of this study aimed to conduct a comprehensive analysis of the opioid overdose research (OOR) landscape, performance, evolution, citation impact and changing research themes.

A bibliometric analysis was performed on the OOR data published between, 1971 and 2024. Data were gathered from the Scopus database and analyzed using Bibliometrix and VOSviewer. Citation counts, prolific authors, top sources, and seminal publications were also identified. Thematic mapping was performed to aid the visualization of the major clusters in the OOR data.

The analysis included 13,971 authors who contributed to the OOR. Prolific authors, such as Walley, A.Y., and Green, T.C., made notable contributions. "Drug and alcohol dependence" emerged as the top source in the publications. The United States exhibited the highest research output, followed by Canada, the United Kingdom, and Australia. The average citation count per article was 22.44, indicating the impact and visibility of the research. Seminal publications have addressed critical topics including opioid prescription patterns, economic burden, medication-assisted therapies, and overdose prevention programs. Thematic mapping revealed clusters related to drug overdose, opioids, overdose prevention, toxicology, buprenorphine, and opioid use disorders.

The findings showed an ongoing need for further studies on gap filling, such as long-term consequences, socioeconomic factors and inequalities, in addition to technology application and interdisciplinary collaboration. By focusing on new themes, as well as longitudinal studies, stakeholders can gain improved knowledge on opioid overdose problem-solving solutions that have been applied to victims and their communities, thereby improving outcomes.

Investigations have highlighted the detrimental neurological outcomes associated with tramadol exposure, yet studies addressing histopathological changes in the cerebellum following prenatal exposure remain limited. Therefore, this study aimed to elucidate alterations in cerebellar architecture induced by tramadol administration during gestation, particularly during the critical period of neuronal differentiation, while evaluating the potential neuroprotective role of L-carnitine.

A cohort of eight male pups was euthanized at two postnatal time points: one and three weeks after birth. Each age group was divided into four experimental categories: Group I (control); Group II (L-carnitine), where pregnant rats received L-carnitine; Group III (tramadol), where offspring from tramadol-exposed mothers were assessed; Group IV (tramadol + L-carnitine), which included pregnant rats administered both tramadol and L-carnitine. Treatments began on gestational day 7 and continued until day 21. Pups were sacrificed on postnatal days 7 and 21 following treatment, and cerebellar samples were subjected to histological and immunohistochemical analyses to evaluate oxidative stress markers. Data were analyzed using GraphPad Prism v7.01 and expressed as the mean ± SEM; significance (p < 0.05) was assessed using a t-test or one-way ANOVA with the Tukey–Kramer post hoc test.

Prenatal tramadol exposure resulted in significant histological alterations in the developing cerebellar cortex of the postnatal offspring. Noteworthy findings included the persistence of the external granular layer, degeneration of Purkinje cells with pericellular halos and vascular congestion, all of which correlated with oxidative stress markers. In contrast, L-carnitine co-administration facilitated a restoration of normative cerebellar architecture.

These findings indicate that tramadol exposure during pregnancy elicits substantial degenerative changes in the cerebellar cortex, highlighting L-carnitine co-treatment as a promising strategy to mitigate these tramadol-mediated adverse effects.

Sacubitril/valsartan sodium tablets (SVSTs) represent a therapeutic option for chronic heart failure (CHF), functioning by inhibiting angiotensin II receptors and neprilysin. Thus, this study aimed to develop mesoporous nano-bioactive glass (MNBG)-loaded SVSTs to enhance the bioavailability of SVSTs and investigate the treatment effects on myocardial cell autophagy and apoptosis in rats with CHF.

The MNBG-loaded SVSTs were prepared and tested in normal Sprague-Dawley rats (Ctrl group) and CHF models created through abdominal aortic ligation. The rats were divided into CHF, SVST, and SVST/MNBG groups (15 rats each). Cardiac function, myocardial tissue pathology, and the levels of reactive oxygen species (ROS), nitric oxide (NO), creatine kinase-MB (CK-MB), N-terminal pro-B-type natriuretic peptide (NT-proBNP), apoptosis-related proteins (Bcl-2 and Bax), and autophagy-related proteins (Atg5, beclin1, p62, and LC3II/I) were assessed. Statistical analysis was performed using SPSS 26.0 via one-way analysis of variance (ANOVA), t-test, and χ² test (p < 0.05).

The CHF group demonstrated reduced cardiac function with increased ROS, CK-MB, NT-proBNP levels, and decreased NO levels, along with altered protein expression (decreased Bcl-2, Atg5, beclin1, p62, and increased Bax, LC3II/I). The SVST and SVST/MNBG groups presented improved cardiac function, reduced ROS, CK-MB, and NT-proBNP levels, increased NO, and favorable protein expression changes. The SVST/MNBG group showed superior improvements compared to the SVST group (p < 0.05).

Loading MNBG with SVSTs can improve cardiac function in CHF models and exert the effects of SVSTs by influencing cardiomyocytes to promote autophagy–apoptosis. These findings provide preliminary evidence for identifying potential candidates to treat heart failure.

Drug-eluting stents (DES) have become a crucial strategy for improving the outcomes of patients with coronary artery disease (CAD). This work aimed to evaluates the therapeutic efficacy of metoprolol-loaded poly (lactic-co-glycolic acid)–poly(trimethylene carbonate)–poly (glycolic acid) (PLGA–PTMC–PGA) DES (Meto-PLGA/PTMC DES) in a rabbit model of CAD.

A total of 30 New Zealand white rabbits (male, weighing 4–6 kg) were randomly divided into three groups: Sham group (chest suturing without intervention), Model group (CAD animal model without DES), and stent group (treatment with the Meto-PLGA/PTMC DES). The blood samples were collected at regular intervals to assess the serum inflammatory markers, cardiac function parameters, hemodynamic parameters and coronary remodeling. Statistical analysis was performed using One-way analysis of variance (ANOVA), followed by a post hoc Tukey’s test to compare the differences between groups (p < 0.05 indicated statistically significance).

The Meto-PLGA/PTMC DES, through its unique co-polymer structure, achieved stable Meto loading in vivo. This stent enabled the gradual release of Meto, thus maintaining sustained drug concentrations and optimizing CAD treatment. The animal experiment results indicated that the sent group (Meto-loaded DES) exhibited markedly lower levels of interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) relative to the model group (p < 0.05). In terms of cardiac function, compared with the model group, the stent group exhibited significantly elevated left ventricular systolic pressure (LVSP), ±dp/dt_max, arterial systolic blood pressure (BPs), and diastolic blood pressure (BPd), along with a marked reduction in left ventricular end-diastolic pressure (LVEDP) compared with the model group (p < 0.05). The coronary tissue morphology in the stent group revealed notably reduced intimal thickness, intimal area and degree of stenosis versus the Model group, with a prominent increase in lumen area (p < 0.05).

The Meto-PLGA/PTMC DES not only effectively provides sustained drug release and exhibits superior mechanical properties and excellent blood compatibility. Animal experiments further validated the crucial role of the Meto-PLGA/PTMC DES in reducing inflammatory responses, improving cardiac function and alleviating coronary artery stenosis.

Tinospora cordifolia has been recognized in Ayurvedic medicine for its antidiabetic properties; however, the role of T. cordifolia in diabetic wound healing remains unexplored. Thus, this study aimed to investigate the diabetic wound-healing potential of the aqueous ethanolic stem extract of T. cordifolia (AETC) in streptozotocin–nicotinamide (STZ–NAD)-induced diabetic rats. The extract was prepared using 70% aqueous ethanol via Soxhlet extraction.

A full-thickness excision wound was created on the dorsal skin of diabetic rats, followed by a 14-day oral treatment with the AETC at low (250 mg/kg) and high (500 mg/kg) doses. Key parameters were assessed, including blood glucose levels, the rate of wound contraction, and epithelization time, alongside the histopathological evaluation of wound tissues.

The AETC treatment significantly reduced blood glucose (p < 0.01), enhanced wound contraction (p < 0.05), and accelerated epithelization (p < 0.05) compared to diabetic controls. The histological analysis revealed improved epidermal regeneration, reduced inflammation, and increased granulation tissue and collagen deposition.

These findings suggest that the AETC can exert glycemic control and promote wound healing in diabetic conditions.