To evaluate the role of matrix-remodeling associated 5 (MXRA5), and tissue inhibitor metalloproteinase 2 (TIMP2) levels in predicting the severity of preeclampsia. Forty-eight pregnant women complicated by preeclampsia, whose ages ranged from 20 to 40 years, in addition to 48 age- and sex-matched normotensive pregnant women, served as the control group included in the study. The placental samples in this study were obtained via cesarean section, frozen immediately in liquid nitrogen, and stored at − 80 °C until the time of assay for subsequent RNA and protein biochemical measurements. There was a statistically significant decrease in the mean MXRA5 level among cases compared with controls (p <0.001 for both). However, there was no statistically significant difference in the mean TIMP2 level between the cases and controls. There was a statistically significant lower mean difference in pAKT-ELIZA among PE patients (0.29±0.04) than among controls (0.56±0.14, p<0.001), with a positive correlation between pAKT and MXRA5. MXRA5 performed high accuracy (sensitivity: 96.7%, specificity: 94.4%) in excluding cases and controls with PE. Furthermore, MXRA5 exhibited greater sensitivity in distinguishing between severe and mild cases (95.5%, sensitivity 96.7%, specificity), whereas the role of TIMP2 was insignificant.
In conclusion: in pre-eclampsia patients, reduced MXRA5 expression is a highly sensitive biomarker for detecting and predicting the severity of PE.
This study evaluated the neuroprotective potential of a combination therapy using liraglutide (LIRA), an antidiabetic agent, and rivastigmine (RIVA), a standard treatment for Alzheimer's disease (AD), in a rat model of aluminum chloride (AlCl₃)‐induced AD. Male rats were divided into five groups: control, AD (AlCl₃,75 mg/kg for 60 days), RIVA‐treated (1 mg/kg daily for 6 weeks), LIRA‐ treated (300 µg/kg daily for 6 weeks), and combination‐treated (LIRA + RIVA). Cognitive function was assessed behaviorally, and hippocampal biomarkers related to AD—such as microtubule‐associated protein Tau (MAPt), Beta‐Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1), Sequestosome 1 (SQSTM1/p62), and acetylcholinesterase (AChE) activity—were evaluated. Histopathological changes, immunohistochemistry, and transmission electron microscopy were also assessed. The levels of MAPt, BACE1, SQSTM1/p62, and AChE in the LIRA + RIVA group were 11.32 ± 0.467 ng/mL, 1069 ± 80.1 pg/mL, 408.7 ± 19.41 pg/mL, and 0.805 ± 0.342 µmol of acetylthiocholine iodide hydrolyzed/min/g of tissue, respectively. These levels were significant (p < 0.01) when compared with the AlCl3 group. Histological findings supported these biochemical data, indicating enhanced neuroprotection. LIRA may have a potential neuroprotective effect due to the rise in AChE, BACE1, (SQSTM1/p62) amyloid beta (Aβ), and caspase‐3 levels induced by AlCl3. Co‐administration of LIRA and RIVA provided superior neuroprotective effects compared with RIVA alone, suggesting a promising therapeutic strategy for preserving cognitive function in AD.
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