Intracerebral hemorrhage (ICH) is associated with high rates of mortality and disability, underscoring an urgent need for effective therapeutic interventions. The clinical prognosis of ICH remains limited, primarily due to the absence of targeted, precise therapeutic options. Advances in novel drug delivery platforms, including nanotechnology, gel-based systems, and exosome-mediated therapies, have shown potential in enhancing ICH management. This review delves into the pathophysiological mechanisms of ICH and provides a thorough analysis of existing treatment strategies, with an emphasis on innovative drug delivery approaches designed to address critical pathological pathways. We assess the benefits and limitations of these therapies, offering insights into future directions in ICH research and highlighting the transformative potential of next-generation drug delivery systems in improving patient outcomes.

Nowadays development of safe and simple siRNA delivery system is still a great challenge. Carbon dots have attracted considerable attention in bioimaging, drug delivery, nanosensors, and other fields during the past few years. In this study, we successfully developed carbon dots (TEPA-CDs) as siRNA nanocarriers based on glucose and tetraethylene pentamine. TEPA-CDs have a mean diameter of less than 10 nm and positive charged decoration. TEPA-CDs could condense siRNA into stable complexes without no obvious premature release. Cellular uptake analysis clearly showed that Cy3-labeled siRNA could be uptake by HeLa cells. GFP expression in HeLa-EGFP cells could be significantly inhibited by TEPA-CDs/siRNA complexes. Our study indicated that TEPA-CDs could be used as a siRNA nanocarrier to tumor cells.

Neuromyelitis optica (NMO) is a severe neurological demyelinating autoimmune disease that affects the optic nerves and spinal cord. There is currently no effective cure or therapy. Aquaporin‑4 (AQP4) is a known target of the autoimmune antibody NMO‑IgG. Therefore, binding of NMO‑IgG to AQP4, and subsequent activation of antibody‑mediated and complement‑dependent cytotoxicity (CDC), are thought to underlie the pathogenesis of NMO. In the present study, a cell‑based high‑throughput screening approach was developed to identify molecular inhibitors of NMO‑IgG binding to AQP4. Using this approach, extracts from the herb Petroselinum crispum were shown to have inhibitory effects on NMO‑IgG binding to AQP4, and the natural compound geraldol was purified from the herb extracts. Analytical high performance liquid chromatography, electrospray ionization‑mass spectrometry and nuclear magnetic resonance analyses confirmed the identity of the isolated compound as geraldol, a flavonoid. Geraldol effectively blocked binding of NMO‑IgG to AQP4 in immunofluorescence assays and decreased CDC in NMO‑IgG/complement‑treated FRTL‑AQP4 cells and primary astrocytes. Geraldol exhibited low cytotoxicity, with no effect on proliferation or apoptosis of FRTL‑AQP4 cells and primary astrocytes. Permeability assays indicated that geraldol did not alter the water transport function of AQP4 in either cell system. The present study suggests the potential therapeutic value of geraldol for NMO drug development.