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The exploitation of drought is a critical worldwide challenge that influences wheat growth and productivity. This study aimed to investigate a synergistic amendment strategy for drought using the single and combined application of plant growth-promoting microorganisms (PGPM) (Trichoderma harzianum) and biogenic silica nanoparticles (SiO2NPs) from rice husk ash (RHA) on Saudi Arabia's Spring wheat Summit cultivar (Triticum aestivum L.) for 102 DAS (days after sowing). The significant improvement was due to the application of 600 ppm SiO2NPs and T. harzianum + 600 ppm SiO2NPs, which enhanced the physiological properties of chlorophyll a, carotenoids, total pigments, osmolytes, and antioxidant contents of drought-stressed wheat plants as adaptive strategies. The results suggest that the expression of the studied genes (TaP5CS1, TaZFP34, TaWRKY1, TaMPK3, TaLEA, and the wheat housekeeping gene TaActin) in wheat remarkably enhanced wheat tolerance to drought stress. We discovered that the genes and metabolites involved significantly contributed to defense responses, making them potential targets for assessing drought tolerance levels. The drought tolerance indices of wheat were revealed by the mean productivity (MP), stress sensitivity index (SSI), yield stability index (YSI), and stress tolerance index (STI). We employed four databases, such as BAR, InterPro, phytozome, and the KEGG pathway, to predict and decipher the putative domains in prior gene sequencing. As a result, we discovered that these genes may be involved in a range of important biological functions in specific tissues at different developmental stages, including response to drought stress, proline accumulation, plant growth and development, and defense response. In conclusion, the sole and/or dual T. harzianum application to the wheat cultivar improved drought tolerance strength. These findings could be insightful data for wheat production in Saudi Arabia under various water regimes. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) has a series of reproductive and metabolic consequences. Although the link between PCOS, IR, and obesity, their impact on the pathogenesis of PCOS has yet to be determined. Dysfunction of PI3K/AKT pathway has been reported as the main cause of IR in PCOS. This study purposed to explore the effects of selenium nanoparticles (SeNPs) alone and combined with metformin (MET) in a PCOS-IR rat model. After 3 weeks of treatment with SeNPs and/or MET, biochemical analysis of glycemic & lipid profiles, and serum reproductive hormones was performed. Inflammatory, oxidative stress, and mitochondrial dysfunction markers were determined colormetrically. The expression of PI3K and Akt genes were evaluated by Real-time PCR. Histopathological examination and Immunohistochemical analysis of Ki-67 expression were performed. The results showed that treatment with SeNPs and/or MET significantly attenuated insulin sensitivity, lipid profile, sex hormones levels, inflammatory, oxidative stress and mitochondrial functions markers. Additionally, PI3K and Akt genes expression were significantly upregulated with improved ovarian histopathological changes. Combined SeNPs and MET therapy could be potential therapeutic agent for PCOS-IR model via modulation of the PI3K/Akt pathway, enhancing anti-inflammatory and anti-oxidant properties and altered mitochondrial functions. The strong relationship between obesity, insulin resistance, and polycystic ovarian syndrome. Disturbance of the PI3K/Akt signaling pathway is involved in the progression of polycystic ovary syndrome-insulin resistance (PCOS-IR). In PCOS-IR rats, combined SeNPs and metformin therapy considerably alleviated IR by acting on the PI3K/Akt signaling pathway. The combination of SeNPs and metformin clearly repaired ovarian polycystic pathogenesis and improved hormonal imbalance in PCOS-IR rats. [ABSTRACT FROM AUTHOR]

This study evaluated possible mitigating effect of adropin on lung injury in diabetic rats, targeting role of Rho A/Rho‐associated kinase pathway. Rats were allocated into four groups: control, adropin, diabetic, and diabetic+adropin groups. At the termination of the experiment, serum fasting glucose, insulin and adropin levels and insulin resistance were calculated. Wet/dry ratio, histopathological, immunohistochemical analyses, and relative real time gene expression of lung tissue was determined. Interleukin‐6, tumor necrosis factor alpha, malondialdehyde, 8‐Oxo‐2′‐deoxyguanosine, reduced glutathione, superoxide dismutase, Bcl‐2, BAX, myeloperoxidase, intracellular adhesion molecule‐1, vascular cell adhesion molecule‐1, and transforming growth factor‐β were determined in lung tissue. Adropin treatment in diabetic rats notably attenuated hyperglycemia and insulin resistance. Also, it mitigated diabetic lung injury via suppressing effect on Rho A/ROCK pathway, apoptosis, inflammatory reactions, oxidative stress, and fibrosis of lung tissue. Adropin can be considered as a promising therapeutic agent for treating diabetic lung injury. [ABSTRACT FROM AUTHOR]

A mechanistic understanding of the dynamic interactions between the mitochondria and the gut microbiome is thought to offer innovative explanations for many diseases and thus provide innovative management approaches, especially in GIT-related autoimmune diseases, such as ulcerative colitis (UC). β-Glucans, important components of many nutritious diets, including oats and mushrooms, have been shown to exhibit a variety of biological anti-inflammatory and immune-modulating actions. Our research study sought to provide insight into the function of β-glucan and/or fidarestat in modifying the microbiome/mitochondrial gut axis in the treatment of UC. A total of 50 Wistar albino male rats were grouped into five groups: control, UC, β-Glucan, Fidarestat, and combined treatment groups. All the groups were tested for the presence of free fatty acid receptors 2 and 3 (FFAR-2 and -3) and mitochondrial transcription factor A (TFAM) mRNA gene expressions. The reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and ATP content were found. The trimethylamine N-oxide (TMAO) and short-chain fatty acid (SCFA) levels were also examined. Nuclear factor kappa β (NF-kβ), nuclear factor (erythroid-2)-related factor 2 (Nrf2) DNA binding activity, and peroxisome proliferator-activated receptor gamma co-activator-1 (PGC-1) were identified using the ELISA method. We observed a substantial increase FFAR-2, -3, and TFAM mRNA expression after the therapy. Similar increases were seen in the ATP levels, MMP, SCFA, PGC-1, and Nrf2 DNA binding activity. The levels of ROS, TMAO, and NF-kβ, on the other hand, significantly decreased. Using β-glucan and fidarestat together had unique therapeutic benefits in treating UC by focusing on the microbiota/mitochondrial axis, opening up a new avenue for a potential treatment for such a complex, multidimensional illness. [ABSTRACT FROM AUTHOR]