ABSTRACT
This study aims to examine the antimicrobial and antioxidant activities of the aerial parts of Chenopodium album extracts (CAE) prepared with different solvents, and how C. album ethanol extract protects them against gentamicin-induced nephrotoxicity. Extracts of C. album aerial parts were obtained from ethanol, water, methanol, chloroform, and hexane solvents. Thirty-two male Wistar albino rats were used and gentamycin-induced nephrotoxicity was utilized as a model. The water extract of C. album exhibited no antimicrobial effect, whereas the methanol one created the highest zone diameter on Bacillus cereus (26 mm). The methanol extract displayed the highest activity in DPPH and ABTS. The ethanol extract yielded the highest reducing power in the CUPRAC. The water extract had the highest reducing power in the FRAP. Concerning gentamicin-induced renal damage, creatinine and urea levels in the blood were statistically higher in the gentamicin-C. album group compared to the other groups (p < .05). Urea and creatinine levels of the gentamicin-C. album group dropped significantly, indicating that the C. album was effective against renal damage. The sections from kidney tissues in the gentamicin + C. album group mostly exhibited mild glomerular congestion. Hyaline cast, cytoplasmic vacuolization, necrosis, and apoptosis were not observed. Thanks to C. album treatment, the gentamicin + C. album suffered less histopathological damage than the gentamicin group did. The results of the present study suggest that CAE can be used as a supportive treatment in people undergoing treatment for nephrotoxicity.
ABSTRACT
Sigma-1 receptor (SIG1R) is a chaperone that modulates inositol 1,4,5-trisphosphate receptor type1 (IP3R1) calcium (Ca2+) channels on the endoplasmic reticulum. Therefore, SIG1R functions as an indirect regulator of Ca2+ and acts as an apoptosis modulator. Increased expression of SIG1R is associated with poor prognosis in breast cancers (BC), and SIG1R antagonists like BD1047 induce apoptosis. As a heavy metal, cadmium (Cd2+) is competitive with Ca2+ due to its physicochemical similarities and may trigger apoptosis at low concentrations. Our study investigated the SIG1R protein expression in 74 BC patients and found a significant increase in SIG1R expression in the triple-negative BC subtype. We also examined the apoptotic and anti-cancer effects of BD1047 in combination with CdCl2 in MCF7 and MDA-MB-213 cells. Cells were treated with CdCl2 at doses of 1 µM, 25 µM, and 50 µM, along with BD1047. Higher doses of CdCl2 were cytotoxic on both cancer cells and significantly increased DNA breaks. However, low-dose CdCl2 with BD1047 increased cell death and the apoptotic index in BC cells, although it did not exhibit cytotoxic effects on HUVEC cells. Co-administration of low-dose CdCl2 with BD1047 also reduced the migration and colony-forming ability of BC cells. Moreover, the expression of SIG1R protein in these groups decreased significantly compared to groups treated with BD1047 or low-dose CdCl2 alone. In conclusion, low-dose CdCl2 is thought to increase the apoptotic ability of BD1047 in BC cells by reducing SIG1R expression.
