Morchella esculenta Pers. (Morchellaceae) was investigated for its antioxidant activity by measuring the intracellular reactive oxygen species in HT-29 colon cancer cells. The methylene chloride extract, which showed the highest antioxidant activity, led to the isolation of four fungal sterols, 1–4, and trilinolein (5), in addition to methyl myristate (6), 1-linoleoylglycerol (7), and ceramide (8). The isolated compounds were identified through the analysis of various spectroscopic methods. In the hydroxyl radical assay, 5-dihydroergosterol exhibited significant antioxidant activity. All compounds isolated were also tested using an enzyme-based Elisa NF-κB assay. Fungal sterols and trilinolein showed significant inhibition of NF-κB activation in the NF-κB assay.

The present study reports ecofriendly synthesis of CuO nanoparticles (NPs) using an extract of Rhus punjabensis as a reducing agent. NPs structural and composition analysis are evaluated by X-rays diffraction (XRD), Fourier transform infrared, Energy dispersive spectroscopy, Scanning electron microscopy, Transmission electron microscopy, and Thermal analysis. The NPs have pure single phase monoclinic geometry with spherical structure and high stability toward heat and with average particle size of about 36.6 and 31.27 nm calculated by XRD and SEM, respectively. NPs are tested for antibacterial, protein kinase (PK) inhibition, SRB cytotoxic, and NF-κB activities. Antibacterial activity is observed against B. subtilis and E. coli. Significant PK and SRB cytotoxic activity is observed with some NF-κB inhibition. NPs IC₅₀ values against HL-60 and PC-3 prostate cancer cells are 1.82 ± 1.22 and 19.25 ± 1.55 μg/mL. The results encourage further studies for antibacterial and anticancer drug development of NPs using animal models.

Background: Prostate cancer presents the highest incidence rates among all cancers in men. Hapalindole H (Hap H), isolated from Fischerella muscicola (UTEX strain number LB1829) as part of our natural product anticancer drug discovery program, was found to be significantly active against prostate cancer cells. Materials and Methods: In this study, Hap H was tested for nuclear factor-kappa B (NF-ĸB) inhibition and selective cytotoxic activity against different cancer cell lines. The apoptotic effect was assessed on PC-3 prostate cancer cells by fluorescence-activated cell sorting analysis. The underlying mechanism that induced apoptosis was studied and the effect of Hap H on mitochondria was evaluated and characterized using western blot and flow cytometric analysis. Results: Hap H was identified as a potent NF-ĸB inhibitor (0.76 μM) with selective cytotoxicity against the PC-3 prostate cancer cell line (0.02 μM). The apoptotic effect was studied on PC-3 cells. The results showed that treatment of PC-3 cells with Hap H reduced the formation of NAD(P)H, suggesting that the function of the outer mitochondrial membrane was negatively affected. Thus, the mitochondrial transmembrane potential was assessed in Hap H treated cells. The results showed that the outer mitochondrial membrane was disrupted as an increased amount of JC-1 monomers were detected in treated cells (78.3%) when compared to untreated cells (10.1%), also suggesting that a large number of treated cells went into an apoptotic state. Conclusion: Hap H was found to have potent NF-ĸB p65-inhibitory activity and induced apoptosis through the intrinsic mitochondrial pathway in hormone-independent PC-3 prostate cancer cells.

Background/Aim: This study aimed to uncover the effects of (+)-betulin on the NF-κB-apoptotic pathway in MDA-MB-231 cells, and determine its toxicity and protein expression in vivo. Materials and Methods: Cell cytotoxicity and toxicity were determined using the SRB assay and a zebrafish model, respectively. Western blot, mitochondrial transmembrane potential (MTP), and computational modeling analysis were performed. Results: (+)-betulin inhibited the growth of MDA-MB-231 cells, but did not induce toxicity in zebrafish. (+)-Betulin inhibited the activity of NF-κB p65 in silico and in vitro. In cells, (+)-betulin down-regulated NF-κB p50 and 65, IKKα and β, ICAM-1 and bcl-2 expressions. Cell co-treatment with (+)-betulin and TNFα increased the (+)-betulin cytotoxic potential. Moreover, (+)-betulin induced the loss of MTP. Furthermore, (+)-betulin, in zebrafish, down-regulated the expression of NF-κB p65, IKKα, ΙΚΚβ and procaspase-3. Conclusion: The results contribute to the understanding of the mode of action on apoptosis induction by inhibiting NF-κB pathway in MDA-MB-231 cells.