The emergence of bacterial strains resistant to available antibiotics due to overprescription has prompted a search for alternative treatments. Among the most promising is baicalin, a flavonoid extracted from the roots of Scutellaria baicalensis. Roots, the primary natural source of baicalin, have been extensively explored using emerging extraction technologies such as ultrasonic-assisted extraction and supercritical fluid extraction. These methods offer significant advantages over traditional reflux extraction for baicalin preparation, including shorter extraction times, lower energy consumption, and improved environmental sustainability. Baicalin exhibits remarkable antibacterial activity in vitro and has demonstrated therapeutic efficacy against gastrointestinal infections, meningitis, pulmonary diseases, and sepsis, among other infectious disorders, in animal models. Documented mechanisms of action include disrupting the Escherichia coli membrane, downregulating quorum-sensing gene expression in Pseudomonas aeruginosa, and inhibiting host inflammatory pathways such as PI3K/Akt/NF-κB. However, its clinical translation faces several bottlenecks, including reliance on animal experiment data, low bioavailability, and regulatory compliance issues. This review compares baicalin extraction yields from different natural sources, summarizes the advantages and disadvantages of various extraction technologies, analyzes possible mechanisms of action in treating different bacterial diseases, and discusses outstanding challenges and best strategies for expanded clinical use against bacterial infection. Our aim is to provide a valuable reference for future research and clinical applications.

Thrombocytopenia is a hematologic disorder characterized by an abnormally low platelet count in peripheral blood. Recent studies have identified mutations in DUT as the primary cause of bone marrow failure and diabetes mellitus syndrome (BMFDMS), a condition commonly associated with thrombocytopenia. In this study, a novel rabbit model of thrombocytopenia carrying the DUT c.3020A>G (p.Y116C) mutation was established using SpRY-ABEmax-mediated base editing. This model accurately recapitulates the clinical manifestations of human thrombocytopenia. Phenotypic analysis has revealed that mutant rabbits exhibited significant reductions in megakaryocyte numbers, platelet counts, and survival rates when compared to wild-type controls. Mechanistic investigations showed that the DUT mutation leads to mitochondrial structural abnormalities and functional impairments. Notably, platelets from DUT (p.Y116C)-mutant rabbits exhibited markedly reduced DUT protein expression and enhanced mitophagy, potentially mediated through the Park2 pathway. This study presents the first genetic model of thrombocytopenia that closely mimics the human DUT (p.Y116C) mutation, offering new insights into the relationship between DUT mutations and platelet function, and highlighting potential therapeutic targets for human thrombocytopenia.

Celastrol (CSL), a natural triterpenoid extracted from Tripterygium wilfordii, demonstrates a wide range of biological activities. In this study, we explored whether CSL alleviates kidney damage in spontaneously hypertensive rats (SHRs) through the modulation of the Nrf2/Ho-1 pathway, a crucial target in renal injury models. A total of 40 male SHRs, aged 6–8 weeks, were randomly allocated to four groups: the control group (CON, serving as the healthy control), the spontaneously hypertensive rat group (SHR), the SHR group treated with low-dose CSL (L-CSL + SHR, 0.5 mg/kg/d), and the SHR group treated with high-dose CSL (H-CSL + SHR, 1 mg/kg/d). All drugs were formulated using physiological saline as the solvent and administered via intraperitoneal injection. The control group received an equivalent volume of physiological saline via intraperitoneal injection, and all groups underwent continuous daily administration for 6 weeks. The results indicated that, in comparison with the control group, the serum levels of angiotensin, angiotensin-converting enzyme, and aldosterone in the SHR group were relatively high, and CSL treatment further downregulated these indices. Simultaneously, CSL downregulated pro-inflammatory factors (tumor necrosis factor-α and interleukin-1β) and upregulated interleukin-6. Regarding renal function-related indicators, CSL reduced malondialdehyde levels and enhanced the activities of antioxidant enzymes, such as superoxide dismutase, glutathione peroxidase, and catalase. Moreover, CSL inhibited the overexpression of Keap1. Significantly, the mRNA levels of Nrf2, Nqo1, and Ho-1 in the CSL-treated groups were notably higher than those in the SHR group. These findings suggest that CSL mitigates renal pathological damage in SHR by activating the Nrf2/Ho-1 pathway, offering a potential therapeutic approach for hypertension-induced renal injury.