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Bilharziasis is a widespread trematode parasite that poses a severe public health burden. Dandelion (Taraxacum officinale) has several pharmacological and traditional properties critical for treating several hepatic disorders. The present study was designed to assess the potential efficacy of T. officinale root (TOR) dietary supplementation with or without praziquantel (PZQ) against liver and intestinal disorders in mice infected with Schistosoma mansoni. This study was conducted on five groups; G1: uninfected control, G2: untreated S. mansoni-infected mice, G3: infected animals treated with 250 mg/kg PZQ for three alternative days, G4: infected animals were orally administered 600 mg/kg bw TOR daily for 10 days, and G5: infected animals that received both PZQ and TOR as previously described. The current findings after different treatments indicated topographical scanning electron microscopy alterations of male adult worms and a critical reduction in worm burden, ova count, granuloma diameter, hepatic and intestinal histological abnormalities, fibrosis, immunohistochemical expression of CD3+ and CD20+ cells, oxidative stress, and interleukin-10, also upregulation of interferon-gamma, and antioxidant enzymes, when compared to the infected untreated mice. The best results were obtained in mice administered PZQ+TOR together because of their antioxidant properties and ability to promote the host immune response to parasitic infection.

Exposure to aluminum chloride (AlCl3) induces progressive multiregional neurodegeneration in animal models by promoting oxidative stress and neuroinflammation. The current study was designed to assess the potential efficacy of the natural antioxidants celastrol and thymoquinone (TQ) for alleviating AlCl3-induced psychomotor abnormalities and oxidative-inflammatory burden in male albino rats. Four treatment groups were compared: (i) a vehicle control group, (ii) a AlCL3 group receiving daily intraperitoneal (i.p.) injection of AlCl3 (10 mg/kg) for 6 weeks, (iii) a AlCl3 plus TQ (10 mg/kg, i.p.) cotreatment group, and (iv) a AlCl3 plus celastrol (1 mg/kg, i.p.) cotreatment group. Open-field, rotarod, and forced swimming tests were conducted to assess locomotor activity, motor coordination, anxiety-like behavior, and depressive-like behavior. Acetylcholine (ACh), dopamine, and serotonin levels were measured in brain homogenates. Malondialdehyde (MDA), total antioxidant capacity (TAC), and catalase activity were measured as oxidative stress markers, while tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) expression levels were measured as inflammatory markers. Brain derived neurotrophic factor (BDNF) mRNA was measured as an index for the endogenous neuroprotective response. Daily AlCl3 injection reduced free ambulation, impaired motor coordination, promoted anxiety- and depression-like behaviors, reduced whole-brain ACh, dopamine, and serotonin concentrations, increased MDA accumulation, reduced TAC, elevated TNF-α and IL-6, and suppressed BDNF mRNA expression. All of these effects were significantly reversed by TQ or celastrol cotreatment. Thus, TQ and celastrol may be promising treatments for AlCl3-induced neurotoxicity as well as neurodegenerative diseases involving oxidative stress and neuroinflammation.

There are many mechanisms of resistance, chemoresistance of HeLa cells to anti-cancer agents seems to be autophagy-mediated. While using very effective anti-cancers such as Doxorubicin and cisplatin, cells overcome the cytotoxicity of these drugs through promotion of what so-called cytoprotective autophagy. Here in this study, we sought to introduce a novel platinum-based compound PBC-II that possesses anti-cancer activity. Our data showed that PBC-II is able to induce apoptosis at relatively low concentrations, with no detectable reactive oxygen species (ROS). However, further experiments demonstrated that exposure of HeLa cells to PBC-II did not promote autophagy; rather, it resulted in accumulation of p62 and decrease in LC3-II levels. Autophagy was then promoted in HeLa cells pharmacologically by Doxorubicin and genetically by siRNA IL-10. In order to confirm promotion of autophagy in our model, we performed acridine orange staining to assess for autophagy under microscope as well as via flow cytometry. We then measured protein level of autophagy markers p62 and LC3 by western blot. Our data indicated that PBC-II interferes with therapy-induced autophagy. We also determined PI3K activity while co-incubation of PBC-II with autophagy inducers. It was clear that PI3K activation decreased when PBC-II was co-administered with autophagy inducers. Collectively, PBC-II exerts unique anti-proliferative effects associated with inhibition of autophagy, which indicates that PBC-II is potentially a promising agent to be used in resistant ovarian tumors. Keywords: Ovarian, Autophagy, Doxorubicin, IL-10, Platinum, HeLa