Prompt Description
Methods: Adult male Wistar rats were subjected to diffuse severe traumatic brain injury (TBI) using the Marmarou weight-drop model under anesthesia. Thirty minutes post-injury, pinocembrin (Pino) was administered intraperitoneally at doses of 25, 50, and 100 mg/kg. Neurological function was assessed using the Veterinary Coma Scale, beam walk, and beam balance tests at baseline, immediately after recovery from anesthesia, and at 24, 48, and 72 hours post-trauma. Cerebrospinal fluid (CSF) samples were collected for ELISA analysis of matrix metalloproteinase-9 (MMP-9), and brain tissues were fixed in 10% formalin for histological evaluation using hematoxylin and eosin staining. Results: Severe TBI induced significant neurological deficits, increased cerebral edema, disruption of blood-brain barrier (BBB) integrity, and impaired balance and motor performance. Treatment with pinocembrin at 25 and 50 mg/kg significantly attenuated these pathological changes compared with controls (p < 0.001). These doses also reduced cerebrospinal fluid MMP-9 levels, which were markedly elevated following TBI.
![You are a world-class visual explanation expert. Please convert this concept into an infographic: [1. Platelets were incubated with acridine yellow (Af) to obtain Af-loaded platelets (Af@Plt), and then incubated with fluorescein diacetate (FDA) to obtain platelets co-loaded with acridine yellow and fluorescein ((Af+Flu)@Plt). 2. (Af+Flu)@Plt were injected into blood vessels and distributed to tumor vessels via blood flow. 3. Under ultrasound stimulation, (Af+Flu)@Plt in tumor vessels were activated and released Af and Flu into the tumor tissue. The released Af and Flu were taken up by tumor cells and tumor-associated macrophages (TAMs). 4. Under ultrasound stimulation, tumor cells and TAMs that had taken up Af and Flu generated a large amount of reactive oxygen species (ROS) inside, resulting in oxidative damage and death, and released Af to surrounding cells. 5. In tumor tissue, low concentrations of Af stimulated M2-type TAMs to exhibit an M1-like anti-tumor phenotype, thereby killing tumor cells. At the same time, Af induced tumor cells to release the 'find me' signal ATP and express the 'eat me' signal CRT on the cell surface, thereby promoting the killing of tumor cells by M1-like phenotype TAMs. In tumor tissue, high concentrations of Af disabled M2-type TAMs, preventing M2-type TAMs from interacting with tumor cells, thereby canceling various pro-tumor functions of M2-type TAMs.]](/_next/image?url=https%3A%2F%2Fpub-8c0ddfa5c0454d40822bc9944fe6f303.r2.dev%2Fai-drawings%2F3o7tkY1PoOleTgaRBMncH8gOaVkX0IO8%2F3ce60887-256f-4fc5-a816-60f7154a1007%2F68e5cec3-79bc-4cbd-8cf9-a9e2df1d9aa2.png&w=3840&q=75)