2-(Benzhydryl sulfinyl)-N-sec-butylacetamide) isolated from fig augmented trastuzumab-triggered phagocytic killing of cancer cells through interface with Fcγ receptor.

The objective of the current study was to extract 2-(benzhydryl sulfinyl)-N-sec-butylacetamide), a novel compound from fig, and then determine its role in enhancing trastuzumab-triggered phagocytic killing of SKOV-3 cancer cells. In this study, Soxhlet was used to extract the compound from the mature and air-dried fig fruits. The production of the isolated extracts was enhanced by using polar and non-polar solvents. Several solvents, such as methanol, ethyl acetate, chloroform, and n-hexane, were used to isolate the effective compound 2-(benzhydryl sulfinyl)-N-sec-butylacetamide) from the organic layer. UV-spectroscopy, FT-IR, 1H-NMR, and 13C-NMR were applied to identify the purified compound. The in vitro and in vivo assays demonstrated that the 2-(benzhydryl sulfinyl)-N-sec-butylacetamide) can increase the activity of the phagocytic cells, via the interaction with FcY receptors, along with trastuzumab, and the pathway can use a model for the therapeutic strategy for effective treatment of ovarian cancer cells.

Methanolic Phoenix dactylifera L. Extract Ameliorates Cisplatin-Induced Hepatic Injury in Male Rats.

This study investigated the ameliorative potential of methanolic date flesh extract (MDFE) against cisplatin-induced hepatic injury. Twenty male rats (weighing 180-200 g) were allocated into four groups: control; date flesh (DF) group (oral 600 mg/kg MDFE for 21 days); Cis group (7.5 mg/kg i.p. at day 16); and date flesh/cisplatin (DF/Cis) group (oral 600 mg/kg MDFE for 21 days and 7.5 mg/kg i.p. at day 16). Hepatic biochemical parameters in sera, and inflammatory and oxidant/antioxidant hepatic biomarkers were estimated. Hepatic histological changes and the immunohistochemistry of cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB), and alpha smooth muscle actin (α-SMA) were assessed. Pretreatment with MDFE decreased Cis-triggered liver biochemical parameters, oxidative stress, inflammatory biomarkers, and histological damage. Moreover, MDFE treatment reduced Cis-induced hepatic NF-κB, COX-2, and α-SMA protein expression. MDFE exerted a hepatoprotective effect when used concomitantly with Cis. Its effect was mediated via its antioxidant and anti-inflammatory ingredients.

Hepatoprotective activity of Uncaria tomentosa extract against sub-chronic exposure to fipronil in male rats.

The effects of fipronil (FPN) on the liver of rats were studied. Rats (n = 6) were treated with 9.7 mg/kg (1/10 of FPN LD50), and other rats (n = 6) received 120 mg/kg of 10% Uncaria tomentosa extract, while a mixture of 9.7 mg/kg FPN and 120 mg/kg of 10% Uncaria tomentosa extract were administered orally to the rats (n = 6) daily for 6 weeks. Body, hepatic weights, liver enzymes, and lipid profile were determined. Hepatic activities of MDA, TNO, TAC, TNF-α, and IL-6 in liver homogenate were measured. Immunohistochemistry of NF-kB and liver histopathology were performed. Fipronil-treated rats had a significant (P = 0.02) lower weight gain. Moreover, relative liver weight was significantly (P = 0.003) increased in FPN-treated rats. Rats administrated with FPN exhibited a significantly (P = 0.02) higher liver enzymes and promoted levels of MDA, TNO, TNF-α, and IL-6 (P < 0.0001) than that in the other groups. Immunostaining of NF-κB was increased (P < 0.0001) in FPN-treated rats. Interestingly, Uncaria tomentosa alone or with FPN decreased the liver immunostaining of NF-κB. In conclusion, FPN produced liver injury through lipid peroxidation and stimulation of NF-κB. However, Uncaria tomentosa combated the oxidative stress and liver damage induced by FPN via inhibition of NF-κB.