PI3K/AKT Signaling Pathway Mediated Autophagy in Oral Carcinoma - A Comprehensive Review.

Oral cancer is the most heterogeneous cancer at clinical and histological levels. PI3K/AKT/mTOR pathway was identified as one of the most commonly modulated signals in oral cancer, which regulates major cellular and metabolic activity of the cell. Thus, various proteins of PI3K/AKT/mTOR pathway were used as therapeutic targets for oral cancer, to design more specific drugs with less off-target toxicity. This review sheds light on the regulation of PI3K/AKT/mTOR, and its role in controlling autophagy and associated apoptosis during the progression and metastasis of oral squamous type of malignancy (OSCC). In addition, we reviewed in detail the upstream activators and the downstream effectors of PI3K/AKT/mTOR signaling as potential therapeutic targets for oral cancer treatment.

Protective Effect of Fucoxanthin on Zearalenone-Induced Hepatic Damage through Nrf2 Mediated by PI3K/AKT Signaling.

Hepatotoxic contaminants such as zearalenone (ZEA) are widely present in foods. Marine algae have a wide range of potential applications in pharmaceuticals, cosmetics, and food products. Research is ongoing to develop treatments and products based on the compounds found in algae. Fucoxanthin (FXN) is a brown-algae-derived dietary compound that is reported to prevent hepatotoxicity caused by ZEA. This compound has multiple biological functions, including anti-diabetic, anti-obesity, anti-microbial, and anti-cancer properties. Furthermore, FXN is a powerful antioxidant. In this study, we examined the effects of FXN on ZEA-induced stress and inflammation in HepG2 cells. MTT assays, ROS generation assays, Western blots, and apoptosis analysis were used to evaluate the effects of FXN on ZEA-induced HepG2 cell inflammation. Pre-incubation with FXN reduced the cytotoxicity of ZEA toward HepG2 cells. FXN inhibited the ZEA-induced production of pro-inflammatory cytokines, including IL-1 ß, IL-6, and TNF-α. Moreover, FXN increased HO-1 expression in HepG2 by activating the PI3K/AKT/NRF2 signaling pathway. In conclusion, FXN inhibits ZEA-induced inflammation and oxidative stress in hepatocytes by targeting Nrf2 via activating PI3K/AKT signaling.

The status of zinc in type 2 diabetic patients and its association with glycemic control.

BACKGROUND: Zinc (Zn) is a trace element that carries antioxidant properties. Deficiency of Zn increases oxidative stress, especially in diabetes. The objective of this study was to assess the relationship between the level of Zn and glycemic control in type 2 diabetes. MATERIALS AND METHODS: A cross-sectional study was carried out in the Department of Medicine at King Abdullah bin Abdulaziz University Hospital, Riyadh, Saudi Arabia, from March 2018 to September 2018. A total of 440 participants were included in the study; 252 of these had type 2 diabetes and 188 were controls. All participants had laboratory investigations including fasting blood sugar (FBS), glycosylated hemoglobin, and lipid profile and Zn levels. These two groups (diabetics and controls) were further divided into Zn deficient group and normal Zn group according to their Zn levels. Data were analyzed by using SPSS software. RESULTS: The mean Zn level was 11.7 + 1.5 in the control group, whereas it was significantly low (9.3 + 1.6) in the diabetic group (P < 0.001). Zn deficiency in the control group was only 6.4%, while in the diabetic group, it was 67.9%, (P ≤ 0.001). The mean ages for the low Zn group and normal Zn group were 40.9 + 12.5 and 37.5 + 10.1, respectively, and the Zn deficient group was higher in age (P = 0.003). There was no significant statistical difference between genders regarding Zn deficiency. Obesity was associated with significantly low Zn levels (P = 0.016). The serum Zn level was significantly negatively associated with FBS and glycated hemoglobin in diabetic participants (P < 0.001). CONCLUSION: Diabetic patients have Zn deficiency compared to normal individuals and poor glycemic control is associated with low Zn levels.

The role of calcium, silicon and salicylic acid treatment in protection of canola plants against boron toxicity stress.

Boron (B) toxicity often limits crop yield and the quality of production in agricultural areas. Here, we investigated the effects of calcium (Ca), silicon (Si) and salicylic acid (SA) on development of B toxicity, B allocation in canola (Brassica napus cultivar Sarw 4) and its role in non-enzymatic antioxidants in relation to yield of this cultivar under B toxicity. Canola seedlings were subjected to four B levels induced by boric acid in the absence or presence of Ca, Si and SA. The results showed that Ca, Si and SA addition ameliorated the inhibition in canola growth, water content (WC), and improved siliqua number, siliqua weight and seed index. The B content in shoots and roots and total B accumulation in the whole plant were increased in control plants under B-toxicity-stress, and these parameters were significantly decreased by addition of Ca, Si and SA. The shoot ascorbate pool (ascorbate, AsA, and dehydroascorbate, DHA), α-tocopherol and phenolics (free and bound) were increased under B toxicity, and were significantly decreased in most cases by addition of Ca, Si and SA, except α-tocopherol, which increased at low B levels (0, 25 and 50 mg kg soil-1). The glutathione content did not obviously change by B stress, while added Ca, Si and SA inhibited its accumulation under B stress. In addition, B toxicity reduced the shoot flavonoids content; however, this reduction was not alleviated by the use of Ca, Si and SA treatments. It could be concluded that growth and yield of canola plants grown under high B concentration improved after external application of Ca, Si or SA.