Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is primarily referred to as ulcerative colitis and Crohn’s disease. As the number of patients suffering from IBD increases, diagnosis and treatment have become pressing yet challenging tasks. A major challenge is that patients with IBD do not exhibit characteristic symptoms, making it difficult to differentiate between IBD and other intestinal abnormalities. Endoscopy is the most conventional method used to diagnose IBD; however, this method is invasive and expensive. Therefore, affordable non-invasive techniques need to be developed for diagnosing IBD, highlighting the need to identify biomarkers specific to the disease. It is now established that the gut microbiome contributes significantly in the development of IBD, and changes in the abundance of various organisms in the gut have been widely explored to identify microbial signatures associated with IBD. This review discusses the current state of knowledge on biomarkers in IBD, with a primary focus on the gut microbiome, associated metabolic signatures, and their links with immunological biomarkers. These biomarkers can help propose an integrative model to better understand the pathophysiology of this complex disease. This integrated approach will also provide insights into potential therapeutic targets for designing appropriate treatment strategies for patients.

Despite significant advances in Parkinson’s disease (PD) treatment, it remains incurable, with limited therapeutic options. Currently, repurposing already tested, safe drugs has emerged as an effective therapeutic strategy against various neurodegenerative diseases, including PD. Using a drug-repurposing approach, the current study investigated the neuroregenerative potential of polysialic acid mimicking compounds, 5-nonyloxytryptamine oxalate (5-NOT) and Epirubicin (Epi), an anti-cancer drug, in 1-methyl-4-phenylpyridinium (MPP+)-treated human neuroblastoma SH-SY5Y cells as a PD model.

The excitotoxic model was established by exposing SH-SY5Y cells to 500 µM of MPP+ and subsequently treating them with the test compounds. The effect of MPP+-induced toxicity on cellular and nuclear morphology, as well as on the expression of neuroplasticity and cell survival proteins, were studied by immunostaining, gelatin zymogram, and Western blot assays.

Treatment with 5-NOT and Epi significantly promoted the survival of MPP+-challenged SH-SY5Y cells and prevented changes in their cellular and nuclear morphology by regulating the expression of microtubule-associated protein (MAP-2) and polysialylated-neural cell adhesion molecule (PSA-NCAM) and NCAM synaptic plasticity proteins. Further, 5-NOT and Epi treatment also protected SH-SY5Y cells by restoring levels of nitric oxide, matrix metalloproteinase, and stress response proteins. Interstingly, 5-NOT attenuated MPP+-induced toxicity in SH-SY5Y cells by regulating the intrinsic protein kinase AKT/BAD apoptotic pathway and the P-38 MAP kinase synaptic plasticity pathway.

These preliminary findings suggest that 5-NOT, as a potential polysialic acid glycomimetic, may serve as a promising drug candidate for targeting neurodegeneration of dopaminergic neurons, a hallmark feature of PD.

This review explores the integration of complexity science—specifically, the biological holographic phenomenon and chaos-fractal theory—with the fundamental principles of traditional Chinese medicine (TCM) to optimize perioperative recovery. It examines how these theories provide a scientific foundation for developing a digital TCM diagnosis and treatment platform. Key topics discussed include the application of digital four-diagnosis technology, visualization of perioperative Yin-Yang states, and artificial intelligence-driven biomarker discovery. By quantifying and digitizing core TCM concepts, this approach enables their incorporation into Enhanced Recovery After Surgery protocols. Ultimately, the review highlights the potential of integrating TCM with Western medicine to advance personalized postoperative management, offering both theoretical insights and practical strategies for improving perioperative care.

Prostate cancer (PCa) often manifests insidiously, with most patients being diagnosed at an advanced stage, leading to a poor prognosis. Early detection of PCa can significantly prolong overall survival by impeding the progression of metastasis. A commonly utilized screening method for detecting PCa is the prostate-specific antigen test. However, since the prostate-specific antigen lacks specificity and sensitivity for PCa identification, there is a paramount urgency to develop precise diagnostic biomarkers for early detection. Extracellular vesicles, known as exosomes, are released by cells into body fluids. Exosomes derived from cancer cells can carry genetic information about the tumor, including DNA, RNA, and proteins, which play crucial roles in tumor initiation, invasion, metastasis, and drug resistance. Studies have indicated that exosomes (including messenger RNAs, microRNAs, long noncoding RNAs and others) can enhance the sensitivity and specificity of PCa diagnosis, indicating their potential for early detection. This review highlights the biological characteristics and functions of exosomes, as well as recent advancements in their use for the diagnosis, prognosis, and treatment of prostate cancer.

Huo Xue Tong Luo Capsule (HXTL) has been clinically used to treat osteonecrosis of the femoral head, osteoporosis, and other bone and joint diseases with promising effects. Our previous study has shown that HXTL can promote osteogenesis in mesenchymal stem cells by inhibiting lncRNA-Miat expression through histone modifications. However, the mechanism by which HXTL treats postmenopausal osteoporosis (PMOP) remains unclear. In this study, we used network pharmacology-based mechanism prediction, molecular docking, and pharmacological validation to investigate the mechanism of HXTL in treating PMOP.

The key candidate targets and relevant signaling pathways of HXTL for PMOP treatment were predicted using network pharmacology and molecular docking analysis. RAW264.7 cells were used for Western blot to validate the predicted mechanistic pathways. The ovaries of mice were surgically removed to simulate PMOP. The effect of HXTL on PMOP was evaluated using tartrate-resistant acid phosphatase staining and immunohistochemical assays in vivo.

Network pharmacology analysis suggested that HXTL interacted with 215 key targets linked to PMOP, primarily affecting the PI3K-AKT signaling pathway. Molecular docking showed that the main components of HXTL exhibited strong binding affinity to NFATc1, p-PI3K, and p-AKT1. Furthermore, our in vitro results confirmed that HXTL suppressed the PI3K-AKT signaling pathway. In vivo, HE and tartrate-resistant acid phosphatase staining results showed that HXTL inhibited osteoclast formation and protected bone mass.

This research demonstrated that HXTL could inhibit osteoclast formation and prevent bone loss induced by ovariectomy in mice by inhibiting the PI3K-AKT signaling pathway. These findings provide important evidence for the clinical application of HXTL in treating PMOP.

Epileptogenesis involves complex mechanisms, including inflammation and apoptosis. Rosiglitazone, a peroxisome proliferator-activated receptor gamma agonist, possesses anti-inflammatory and neuroprotective properties. This study investigated whether rosiglitazone can prevent pentylenetetrazole (PTZ)-induced kindling in mice by modulating inflammatory cytokines and apoptosis pathways.

Male C57BL/6 mice (n = 8 per group) were assigned to sham, control, or rosiglitazone-treated groups. Kindling was induced with intraperitoneal PTZ (40 mg/kg) every 48 h for 17 days. Rosiglitazone (0.1 mg/kg) was administered 30 m before each PTZ injection. Seizure progression was monitored, and hippocampal tissues were analyzed via immunohistochemistry and Western blotting to assess cytokine levels (interleukin (IL)-10, IL-17A, tumor necrosis factor-alpha, interferon-gamma), caspase-3 activity, and glial fibrillary acidic protein expression.

Rosiglitazone significantly delayed seizure progression, reduced seizure scores, and lowered pro-inflammatory cytokine levels (IL-17A, tumor necrosis factor-alpha, interferon-gamma) while increasing IL-10. Immunohistochemical analysis revealed fewer caspase-3-positive cells and reduced glial fibrillary acidic protein expression in the treatment group compared to controls.

Rosiglitazone exerts neuroprotective effects in PTZ-induced kindling, likely through its anti-inflammatory and anti-apoptotic actions. These findings underscore its potential as a therapeutic agent for mitigating epileptogenesis, warranting further investigation in combination therapies and clinical trials.

Oxidative stress could be a key process in acyclovir (ACV)-induced nephrotoxicity. N-acetylcysteine (NAC) is a water-soluble antioxidant with anti-inflammatory activity. This study aimed to evaluate the protective effect of NAC on ACV-induced nephrotoxicity in adult Wistar rats.

Forty adult male Wistar rats (200–220 g) were used. The rats were randomly divided into eight groups (n = 5/group) and were treated intraperitoneally daily for seven days as follows: Group 1 (Control) was administered water (0.2mL), while groups 2–4 were administered NAC (25, 50, and 100 mg/kg). Group 5 was administered ACV (150 mg/kg), while groups 6–8 were supplemented with NAC (25, 50, and 100 mg/kg) prior to treatment with ACV (150 mg/kg). On day 8, the rats were weighed and euthanized, and blood samples were collected for the assessment of biochemical markers. The kidneys were weighed and subjected to oxidative stress markers and histological evaluations.

ACV had no significant (p > 0.05) effects on the body and kidney weights of rats compared to the control. ACV produced significant (p < 0.001) elevations in kidney malondialdehyde, serum urea, creatinine, and uric acid levels in rats, which differed from the control. There were significant (p < 0.001) decreases in kidney glutathione, superoxide dismutase, peroxidase, and catalase, as well as serum chloride, potassium, bicarbonate, and sodium levels in ACV-treated rats compared to the control. ACV caused widening of Bowman’s space and tubular necrosis in the kidneys of rats. Nonetheless, NAC supplementation abrogated ACV-induced nephrotoxicity in a dose-dependent manner. Kidney histology was restored by NAC supplementation.

NAC protected against ACV-induced nephrotoxicity. This finding shows that NAC may have therapeutic potential for nephrotoxicity caused by ACV.

Escalating antimicrobial resistance is a global threat, emphasizing the need to explore alternative treatment options. Hence, we aimed to explore the in-vitro activity of ceftazidime-avibactam (CAZ-AVI) in clinical isolates of carbapenem-resistant gram-negative bacteria.

This was an observational, cross-sectional study conducted at the Microbiology Department of Indus Hospital, Karachi, Pakistan, from January 2023 to October 2024. Carbapenem-resistant gram-negative rods isolated from clinical specimens received from the outpatient, emergency, and inpatient departments were included. Consecutive, non-probability sampling was employed for the collection of isolates. Identification of the organisms was confirmed using API® ID strips, and antimicrobial susceptibility for carbapenems and CAZ-AVI was determined via the Kirby-Bauer disc diffusion method.

A total of 158 bacterial isolates were characterized as carbapenem-resistant. Of these, 92 (58%) were Enterobacterales, and 66 (42%) were Pseudomonas aeruginosa. CAZ-AVI was susceptible in 17 (11%) of the isolates, of which four (24%) were Klebsiella spp. and Escherichia coli each, and nine (52%) were P. aeruginosa. CAZ-AVI-susceptible strains were predominant among patients aged 26–50 years (n = 6; 35%), most of whom were females (n = 10; 59%) and inpatients (n = 8; 47%). Clinical samples from patients with urinary tract infections grew the most CAZ-AVI-susceptible strains (n = 9; 53%).

Our study demonstrated low CAZ-AVI susceptibility in our carbapenem-resistant gram-negative bacterial strains. Understanding regional antimicrobial patterns in multidrug-resistant bacteria is crucial for the effective use of CAZ-AVI, along with the strict implementation of strategies for controlling antimicrobial resistance.