Mixed stroke, also known as hemorrhagic infarction or infarction with hemorrhage, presents as a cerebral infarction combined with intracerebral hemorrhage (ICH) on computed tomography (CT) brain scans. ICH is a brain parenchymal hemorrhage caused by the loss of vascular integrity, which can lead to permanent disability or death. The early growth response 2 (EGR2) gene has been studied in a variety of brain diseases. However, effective treatments are still lacking. Methods: In this study, a cell model was constructed using oxyhemoglobin (OxyHb), and cell viability was detected using CCK-8. The mitochondrial membrane potential was measured using a mitochondrial membrane potential detection kit. Protein stress was used to assess the expression of EGR2, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like (BNIP3L or BNIP3L/NIX), and autophagy-related proteins. RT-qPCR detected the expression of EGR2 and BNIP3L mRNA. Microtubule-associated protein 1 A/1B-light chain 3 (LC3) expression was detected by immunofluorescence. Results: This study found that OxyHb reduced microglial viability in a concentration-dependent manner, and 20 μM OxyHb produced the most robust effect and was selected for subsequent experiments. In the cell model, the membrane potential of microglia decreased, and the fluorescence intensities of autophagy-related proteins (ATG7, LC3 II/LC3 I, and P62) and LC3 were inhibited. Over-expression-EGR2 (oe-EGR2) can increase the membrane potential of microglia and promote the fluorescence intensity of autophagy-related proteins (ATG7, LC3 II/LC3 I, and P62) and LC3. Mitochondrial division inhibitor-1 (Mdivi-1) and sh-BNIP3L could reverse the effect of oe-EGR2. Conclusion: EGR2 promotes microglial mitophagy by upregulating BNIP3L, thereby alleviating ICH.
Background: The Plantaris tendon is a viable option for tendon grafting in various reconstructive procedures. This study aimed to develop a predictive model estimating plantaris tendon length (PTL) based on lower leg length (LL) to provide a preoperative baseline reference. Methods: An investigation was conducted on 238 lower limb sides from Thai cadavers to determine the prevalence and morphometry of the plantaris muscle. Measurements included PTL, tendon width (PTW), muscle belly length (PBL), total muscle length (PML), and LL. Results: The plantaris muscle was present in 88.24% of lower limb sides. A significant correlation was observed between PTL and LL (r = 0.581, p < 0.001). The predictive equation established was: PTL (mm) = 79.167 + [0.574 × LL (mm)], with a standard error of estimate of 20.06 mm. Testing on a separate sample showed no significant difference between predicted and actual PTL values (p = 0.206). Out of the 179 sides measured, 64.80% met the criteria for tendon graft suitability. Conclusions: These findings indicate that LL serves as a practical surface measurement providing an approximate preoperative estimate of PTL in a Thai population. Due to its moderate predictive power, it should be used as a supplementary assessment rather than a sole planning tool for surgical applications.
The primary objective of this study was to analyze the potential influence of vitamin D on microglial phenotypic transformation in cerebral hemorrhage. To simulate cerebral hemorrhage conditions, a hemin-induced brain hemorrhage cell model was established, and cell viability was subsequently measured by CCK-8 assay. Western blotting was then performed to detect the expression of P2X7R, NLRP3, and microglial phenotypic transformation marker proteins. The expression of CD16/32 and CD206 was assessed by immunofluorescence, and ELISA was used to measure levels of inflammatory cytokines, including IL-4, TNF-α, IL-1β, IL-10, and IL-6. Vitamin D exhibited a stimulating effect on cell proliferation, reduced the expression of CD16/32 and iNOS, and boosted the expression of CD206, Arg-1, and Iba-1. Moreover, vitamin D inhibited TNF-α, IL-1β, and IL-10 levels and elevated IL-4 and IL-6 levels. This implies that vitamin D can suppress pro-inflammatory phenotypic transformation and promote anti-inflammatory phenotypic transformation in microglia. Additionally, vitamin D suppressed the expression of P2X7R and NLRP3. The effect of P2X7R inhibitor (A438079) treatment was comparable to that of vitamin D, with the addition of vitamin D further enhancing the effect. Vitamin D was found to regulate microglial phenotypic transformation through the P2X7R/NLRP3 signaling pathway, thereby promoting anti-inflammatory and inhibiting pro-inflammatory phenotypic transformation. This finding may lead to new therapeutic strategies for the treatment of ICH-related brain injury.