Kidney disorders have become a prevalent global public health crisis, accompanied by soaring morbidity and insufficient therapeutic regimens in clinical practice. Celastrol, a biologically active pentacyclic triterpenoid isolated from Tripterygium wilfordii, is well documented to exert powerful anti-inflammatory, antioxidant, and anti-fibrotic bioactivities. A growing body of preclinical data confirms that celastrol yields remarkable renoprotective outcomes in a broad spectrum of renal disease models, encompassing diabetic kidney disease, IgA nephropathy, chronic kidney disease, as well as acute kidney injury. Mechanistically, celastrol alleviates renal inflammatory infiltration, oxidative stress injury, and pathological fibrotic remodeling through the synergistic regulation of pivotal signaling axes, such as PI3K/Akt/NF-κB, p38 MAPK/NF-κB, Nrf2/GPX4, and SIRT1/EZH2/Wnt/β-catenin pathways. However, a narrow therapeutic index and systemic toxicity greatly hinder its clinical translation. To address this, kidney-targeted delivery systems-including nanoparticle-based carriers (e.g., liposomes) and microneedle patches-have been developed to increase renal drug accumulation and reduce off-target toxicity. Further efforts should focus on elucidating context-dependent mechanisms, optimizing carrier design, and advancing clinical trials to fully unlock the therapeutic potential of celastrol against kidney diseases.

Leishmaniasis remains a major neglected tropical disease affecting millions of people worldwide, particularly in resource-limited regions where effective prevention and treatment options are often inaccessible. Current control strategies primarily rely on chemical insecticides for sandfly management and antileishmanial drugs for disease treatment. However, the emergence of insecticide and drug resistance, treatment-associated toxicity, environmental contamination, and limited affordability has created an urgent need for safer and more sustainable alternatives. In this context, plant-derived bioactive compounds have gained increasing attention as eco-friendly tools for the management of vector-borne diseases. Azadirachta indica A. Juss. (Neem) is a medicinal plant extensively used in traditional healthcare systems and recognized for its diverse pharmacological properties. This review critically examines the available literature on the efficacy of neem-derived products against sandfly and Leishmania spp. Growing evidence highlights neem as a unique dual-action intervention capable of targeting both the parasite and its vector, making it an attractive candidate for integrated leishmaniasis control. Nevertheless, challenges related to standardization, bioavailability, safety evaluation, and clinical validation remain substantial barriers to translation. Future integration of computational drug discovery, nanotechnology-based formulations, and multidisciplinary experimental approaches may facilitate the development of neem-based therapeutics and vector control strategies for sustainable leishmaniasis management.

Objective: To investigate the efficacy of ginkgolide B, a major active constituent isolated from Ginkgo biloba, on pancreatic β-cell integrity and Nrf2/Keap1 signaling in a streptozotocin (STZ)-induced diabetes model of rats.
Methods: Sprague-Dawley rats were injected with STZ along with nicotinamide. After confirmation of hyperglycemia, diabetic rats (n=8/group) received no treatment, or ginkgolide B (10 or 30 mg/kg). Healthy rats served as normal control. After 21 days of treatment, rats were sacrificed, and plasma samples was obtained to assess the biochemical, hepatic, renal, oxidative stress, lipid profile, apoptotic, and inflammatory parameters. Pancreatic tissue was used for histopathological observation and detection of gene expression of NFE2L2, KEAP1, NQO1, HO-1, Ins1, MAFA, Ngn3, Pdx1, and Pax4.
Results: Ginkgolide B-treated rats showed significant improvement in diabetes markers, i.e., fasting plasma glucose, insulin, and glucagon. It also significantly improved oxidative stress, inflammation, as well as lipid profile, antiapoptotic, liver, and kidney function markers as compared with the model group. Ginkgolide B improved β-cell function, activated Nrf2 signaling, and upregulated β-cell-related genes Ins1, Pdx1, MAFA, Ngn3, and Pax4. Histopathological results showed nearly normal islet architecture in ginkgolide B-treated groups.
Conclusions: Ginkgolide B shows antidiabetic effect. It can alleviate oxidative damage and inflammation, and upregulate genes related to regeneration and insulin signaling.

Objective: To construct an oncolytic herpes simplex virus oHSV-BJ-2 and to evaluate its safety and antitumor efficacy. Methods: Using the HSV-1 wild-type KOS strain as the backbone, we constructed an oncolytic herpes simplex virus, oHSV-BJ-2. The CCK-8 method was used to detect the killing effect of the virus on eight tumor cell lines, and the in vivo tumor inhibitory effect of the virus was evaluated in the BALB/c nude mouse subcutaneous transplant tumor model (PANC-1, SW1990). Results: oHSV-BJ-2 showed a significant killing effect on seven tumor cell lines in a time- and dose-dependent manner. In the PANC-1 and SW1990 pancreatic cancer xenograft tumor models, intratumoral injection of oHSV-BJ-2 could significantly inhibit tumor growth, with the tumor inhibition rate reaching 70%-80% in the medium and high-dose groups, without a significant impact on the body weight of the mice. Conclusions: oHSV-BJ-2 has good safety and significant antitumor activity, and could be explored as a new drug candidate for the treatment of pancreatic cancer and other malignant tumors.