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Abstract Background liver cancer is one of the most common cancers in the world. So far, there is no gold standard treatment for hepatocellular carcinoma. We conducted this in vitro study to assess the effect of three natural products: Boswellic acids, curcumin and naringin versus corresponding nanoparticles (NPs) on Hep G2 cells proliferation. Methods Boswellic acid, curcumin, naringin-loaded NPs were prepared using nanoprecipitation method. Human liver (HepG2) cell line was cultured in Dulbecco’s modified Eagle’s medium (DMEM). The cell growth inhibition and cytotoxicity were evaluated by MTT assay. Results Boswellic acid, curcumin, naringin were able to inhibit HepG2 cells proliferation. IC50 at 24 h, 48 h showed significant lower values in NPs versus Free herbs. IC50 values of free Boswellic acids and NPs at 24 h were (24.60 ± 1.89 and 7.78 ± 0.54, P

Objectives This study aimed to evaluate the potential mitigating effect of fisetin on monosodium glutamate (MSG)-induced testicular toxicity and investigate the possible involvement of silent mating type information regulation 2 homolog 1 (SIRT1) in this effect.Methods Forty male rats were divided into normal control, fisetin-treated, MSG-treated, and fisetin + MSG-treated groups. Testosterone, GnRH, FSH, and LH were measured in plasma, as well as SIRT1 and phosphorylated AMP-activated protein kinase (pAMPK) levels in testicular tissues using ELISA. Hydrogen peroxide (H2O2), nitric oxide (NO), and reduced glutathione (GSH) were measured colorimetrically, while Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) expression was relatively quantified using RT–PCR in testicular tissues.Results After 30 days, fisetin could ameliorate MSG-induced testicular toxicity by acting centrally on the hypothalamic-pituitary-gonadal axis, increasing plasma levels of GnRH, FSH, LH, and testosterone. Peripheral actions of fisetin on the testis were indicated as it increased testicular SIRT1 and pAMPK. Furthermore, it antagonized glutamate-induced oxidative stress by significantly lowering H2O2, NO, and relative NOX4 expression while significantly increasing reduced GSH levels. It also improved the architecture of the seminiferous tubules, reduced sperm abnormality, and increased sperm count.Discussion Fisetin ameliorates MSG-induced testicular toxicity via central and peripheral mechanisms making it a promising therapeutic target for male infertility.

Background: Activation of the NLRC4 inflammasome appears to start many signalling processes inside the host, including caspase-1, the principal protease responsible for converting proIL-1β and IL-18 to active, secreted IL-1β and IL-18, resulting in pyroptosis. Aims: To evaluate NLRC4 level in patient's blood serum to highlight its role in the pathogenesis of leprosy. Materials and Methods: This prospective study was conducted on 40 patients with leprosy and 30 healthy individuals of matched ages and sexes. All patients were subjected to complete history taking, general and dermatological examination, laboratory investigations, slit skin smear with bacillary index, and clinical classification of the studied leprosy group patients regarding disability according to disability grading. And finally, measurement of serum NLRC4 level by ELISA. Results: In the paucibacillary (PB) group, NLRC4 serum level ranged from 0.9 to 1.8 ng/ml with 1.43 ± 0.28 ng/ml, while in the multibacillary (MB) group, it ranged from 1.2 to 5.7 ng/ml with 2.83 ± 1.11 ng/ml. NLRC4 serum level had increased significantly in MB patients compared to PB patients (P < 0.05). There was a significant difference among the three studied groups, regarding the serum level of NLRC4 (P < 0.05). In leprosy patients, significant positive correlations were found between serum levels of NLRC4 and bacillary index and duration of leprosy. Conclusions: Leprosy patients had considerably greater serum levels of NLRC4 than controls. It was much greater in MB patients than in PB patients.