Anti-inflammatory and antioxidant properties of betaine protect against sepsis-induced acute lung injury: CT and histological evidence.

The aim of this research was to determine the anti-inflammatory effect of betaine on sepsis-induced acute respiratory distress syndrome (ARDS) in rats through histopathological examination, radiologic imaging, and biochemical analysis. Eight rats were included in the control group, and no procedure was performed. Feces intraperitoneal procedure (FIP) was performed on 24 rats to create a sepsis-induced ARDS model. These rats were separated into three groups as follows: FIP alone (sepsis group, n=8), FIP + saline (1 mL/kg, placebo group, n=8), and FIP + betaine (500 mg/kg, n=8). Computed tomography (CT) was performed after FIP, and the Hounsfield units (HU) value of the lungs was measured. The plasma levels of tumor necrosis factor (TNF)-α, interleukin-1ß (IL-1ß), IL-6, C-reactive protein, malondialdehyde (MDA), and lactic acid (LA) were determined, and arterial oxygen pressure (PaO2) and arterial CO2 pressure (PaCO2) were measured from an arterial blood sample. Histopathology was used to evaluate lung damage. This study completed all histopathological and biochemical evaluations in 3 months. All evaluated biomarkers were decreased in the FIP + betaine group compared to FIP + saline and FIP alone (all P<0.05). Also, the parenchymal density of the rat lung on CT and histopathological scores were increased in FIP + saline and FIP alone compared to control and these findings were reversed by betaine treatment (all P<0.05). Our study demonstrated that betaine suppressed the inflammation and ameliorated acute lung injury in a rat model of sepsis.

Adipose-derived mesenchymal stem cells mitigate methotrexate-induced liver cirrhosis (fibrosis) model.

OBJECTIVE: Hepatic fibrosis is a severe liver condition characterized by abnormal fibroblast activity, excessive extracellular matrix deposition, inflammation, and structural alterations. Methotrexate (MTX), a pharmaceutical agent widely used for its therapeutic properties, is known to induce hepatotoxicity. However, the precise mechanisms underlying MTX-induced liver injury remain elusive. This study investigates the therapeutic potential of Adipose-Derived Mesenchymal Stem Cells (ADMSCs) in alleviating MTX-induced liver injury in a rat model. MATERIALS AND METHODS: Thirty male Wistar albino rats were employed in this study. Liver injury was induced in twenty rats by a single MTX dose, while ten rats constituted the control group. The MTX group was further subdivided into two cohorts, one receiving ADMSC treatment and the other saline solution. The treatment duration was 14 days. ADMSCs, isolated from adipose tissue, were characterized by CD13, CD29, and CD105 markers. Biomarker analysis, histopathological evaluations, and various measurements were conducted to assess ADMSCs' therapeutic efficacy. RESULTS: MTX administration significantly increased Transforming Growth Factor-ß (TGF-ß), Platelet-Derived Growth Factor (PDGF), Plasma Cytokeratin 18, Plasma Malondialdehyde (MDA), and Liver MDA levels, with histopathological liver damage. ADMSC treatment notably lowered TGF-ß, PDGF, Plasma Cytokeratin 18, Plasma MDA, and Liver MDA levels, accompanied by reduced liver damage observed histologically. Liver Enzyme ALT levels were also reduced in the MTX and ADMSC groups compared to the MTX and Saline groups. CONCLUSIONS: ADMSCs exhibit significant potential in ameliorating MTX-induced liver injury, with notable anti-oxidative and anti-apoptotic properties. These findings suggest that ADMSCs may effectively mitigate oxidative stress and inflammation associated with MTX-induced liver damage. Further research is essential to investigate the clinical application of ADMSCs in liver disease management and uncover the underlying therapeutic mechanisms.

Anti-inflammatory and antioxidant properties of betaine protect against sepsis-induced acute lung injury: CT and histological evidence

The aim of this research was to determine the anti-inflammatory effect of betaine on sepsis-induced acute respiratory distress syndrome (ARDS) in rats through histopathological examination, radiologic imaging, and biochemical analysis. Eight rats were included in the control group, and no procedure was performed. Feces intraperitoneal procedure (FIP) was performed on 24 rats to create a sepsis-induced ARDS model. These rats were separated into three groups as follows: FIP alone (sepsis group, n=8), FIP + saline (1 mL/kg, placebo group, n=8), and FIP + betaine (500 mg/kg, n=8). Computed tomography (CT) was performed after FIP, and the Hounsfield units (HU) value of the lungs was measured. The plasma levels of tumor necrosis factor (TNF)-α, interleukin-1β (IL-1β), IL-6, C-reactive protein, malondialdehyde (MDA), and lactic acid (LA) were determined, and arterial oxygen pressure (PaO2) and arterial CO2 pressure (PaCO2) were measured from an arterial blood sample. Histopathology was used to evaluate lung damage. This study completed all histopathological and biochemical evaluations in 3 months. All evaluated biomarkers were decreased in the FIP + betaine group compared to FIP + saline and FIP alone (all P<0.05). Also, the parenchymal density of the rat lung on CT and histopathological scores were increased in FIP + saline and FIP alone compared to control and these findings were reversed by betaine treatment (all P<0.05). Our study demonstrated that betaine suppressed the inflammation and ameliorated acute lung injury in a rat model of sepsis.