Investigation of neuroprotective and therapeutic effects of cannabidiol in an acute coronary syndrome model.

PURPOSE: The ischemia-reperfusion (I/R) injury seen in the heart can cause severe damage to essential organs such as the brain. Cannabidiol (CBD) obtained from Cannabis sativa is used today to treat various diseases. This study aimed to demonstrate CBD's neuroprotective and therapeutic properties in rats with brain damage caused by I/R in the heart. MATERIALS: Rats were divided into four groups; sham, I/R, I/R + Prophylactic CBD, and I/R + Therapeutic CBD. End of the experiment, brain tissues were collected for biochemical, histopathological, and genetic examinations. RESULTS: I/R damage increased the number of degenerative neurons, caspase-3 and TNF-α immunoexpression, total oxidant status levels, and oxidative stress index. Both prophylactic and therapeutic CBD administration reduced these increased values. In addition, the relative fold changes of AMPK, PGC-1α, SIRT1, and Bcl 2 decreased in the I/R group, and the relative fold change of Bax increased, which are indicators of ER stress and apoptosis. Both administrations of CBD reversed these genes' relative fold changes. CONCLUSION: CBD can be protective against brain injury caused by cardiac I/R damage through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.

Beneficial Effects of Selenium on Kidney Injury via Nf-Kb and Aquaporin-1 Levels.

Systemic inflammation is a serious condition that can affect various tissues and organs, such as the kidneys, and can be life-threatening. Selenium (Se) is an antioxidant and anti-inflammatory trace element. In this study, we aimed to examine the effects of Se, which has antioxidant and anti-inflammatory properties, on lipopolysaccharide (LPS)-induced kidney damage to maintain aquaporin-1 (AQP-1) levels. Four experimental rat groups (n = 8) consisting of the control, LPS alone, LPS + Se, and Se alone were so applied for 7 consecutive days. Upon sacrifice, histopathological results, diagnostic markers of kidney functions, oxidative stress, and inflammation were analyzed. Our results showed that LPS induced mononuclear cell infiltration, cellular residue, and protein deposition in the kidney proximal tubules, and also decreased total antioxidant status levels and increased total antioxidant status and oxidative stress index values. LPS increased the level of creatinine, increased the level of Nuclear Factor kappa B, which has an important role in the inflammation process, and decreased the levels of AQP-1 due to the damage it caused. Se has shown its effect by reversing all these situations. This data suggests that Se can be used as an additive to mitigate LPS-induced toxicity in the kidney.

Protective role of nebivolol via AKT1/Hif-1α/eNOS signaling pathway: nephrotoxicity caused by methotrexate in a rat model.

Methotrexate (MTX) is an antineoplastic and anti-inflammatory agent, which is used in severe diseases. Its use should be limited due to side effects such as nephrotoxicity, myelotoxicity, and hepatotoxicity. Nebivolol (NBV), which is a beta-blocker used in the treatment of hypertension, also contributes to vasodilation in tissues by activating the endothelial nitric oxide synthase (eNOS) enzyme. The purpose of this study is to research the effect of NBV on MTX-induced nephrotoxicity through the AKT1/hypoxia-inducible factor 1-alpha (Hif-1α)/eNOS signaling pathway. The rats were randomly divided into three groups of eight each. The groups were control, MTX, and MTX + NBV. A single dose of 20 mg/kg MTX was given intraperitoneally to the rats on the first day of the study and 10 mg/kg NBV was given orally to the treatment group for 7 days. At the end of the study, rats' blood and kidney tissues were taken for histopathological, immunohistochemical, and biochemical examinations. MTX administration significantly decreased the expression levels of AKT1, eNOS, and Hif-1α compared with the control group (p < 0.001 for all), and NBV treatment increased these values compared with the MTX group (p < 0.001 for all). In conclusion, NBV treatment ameliorated the MTX-induced nephrotoxicity via AKT1/Hif-1α/eNOS signaling pathway.