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Ulcerative colitis (UC) is one of the inflammatory bowel diseases (IBD) that result in recurrent inflammation plus ulcers of the colon and rectum. Recently, mesenchymal stem cell-derived exosomes MSC-EXs have shown a lot of promise for the treatment of gut disorders, with cell regeneration and angiogenesis. Green tea polyphenols (GTPs) display specific beneficial effects on health and pathologies. The aim of this study was to explore the possible effect of MSC-EXs and GTPs on acetic acid-induced UC in rats. Sixty adult male rats were divided into five groups: group I, control group; group II, UC; group ΙIΙ, UC treated with GTPs; group ΙV, UC treated with MSC-EXs; and group V, UC treated with combined GTPs and MSC-EXs. Colonic samples were processed for histological and immunohistochemical methods. Expression of CXCR2 and TLR4 levels was measured. Groups ΙI and III showed ulceration, loss of surface columnar epithelium, disturbed crypt architecture with few goblet cells, and many cellular infiltrations with the overexpression of CXCR2 and TLR4. Group IV showed attenuation of some histological changes. Group V showed improvement of the most histological and immunohistochemical changes described previously. MSC-EXs represent future therapeutic hopes for chronic intestinal inflammatory states, keeping the integrity of innate immunity through their regenerative and anti-inflammatory effects. The combination of GTPs and MSC-EXs was more effective and produced an additive effect than using MSC-EXs alone.

Background: Chronic kidney disease (CKD) leads to a progressive decline in kidney function that eventually progresses to end-stage renal disease. It is critical to identify people at risk for renal disease and to intervene early to avoid kidney damage. Tryptophan hydroxylase (TPH-1) is an accurate biomarker for CKD early stage. The loss of tryptophan hydroxylase contributes to kidney injury. N-acetylcysteine, glycine, and tryptophan can arrest renal fibrosis development and progression through the anti-fibrotic effect of tryptophan hydroxylase and the protective effect of N-acetylcysteine. Objectives: This study aims to assess the metabolic effect of N-acetyl-l-cysteine on kidney function as an EGFR inhibitor and its effect on AAs depletion. In addition, to evaluate the effect of glycine and tryptophan on kidney injury and renal fibrosis progression. Results: Eight weeks of administration of pemetrexed led to a significant increase in serum, urea, creatinine, and uric acid. Administration of N-acetylcysteine (NAC with pemetrexed) resulted in a significant decrease in biochemical kidney function. Also, glycine and tryptophan directly affect renal function; increased expression of tryptophan hydroxylase with decrease expression of EGFR and transforming growth β (TGF-β), compared to N-acetylcysteine group. Conclusion: N-acetylcysteine, glycine, and tryptophan can halt the depletion of AAs in the presence of urea and EGFR. Glycine and tryptophan both have a direct effect on renal function due to their uric acid-lowering properties.

Background: MiRNAs are critical in the course and prognosis of the disease and may aid in developing innovative therapies. Due to miRNAs instability and complicated environment, which includes in vivo degradation by nucleases, deregulation of miRNA expression is the hallmark of liver cancer. MiRNAs can function as oncogenes or tumor suppressors; miRNA-222 promotes tumor progression by cancer-related biological processes. MiRNAs are a novel method for cancer gene therapy due to their influence on cell signaling pathways by inhibiting or promoting many related genes. The interaction between genetics and cellular pathways contributes significantly to the onset and progression of HCC This study aims to illustrate molecular insights into the biological basis of potential anticancer efficacy of anti-microRNA in HCC cell lines Results:Normalization of dysregulated miRNAs by down-regulation block HCC cell proliferation or increase the sensitivity of liver cancer cells to chemotherapy. Effect of UTMD-mediated with anti-microRNA-222 leads to cell proliferation inhibition and cell apoptosis induction in HepG2 cells line. Inhibition of miR222 expression leads to cell cycle arrest and activation of its target genes. Conclusion: Ultrasound microbubbles are frequently utilized to investigate gene and miRNA functions. Gene delivery of miR-222 inhibitor by microbubbles/ultrasound is a new therapy and overcome chemotherapy side effects.

Amoxicillin/ Clavulanate (AC) combination has become one of the antibiotics most widely prescribed used in the treatment of several bacterial infections, might be associated with liver injury. This study was aimed to investigate amoxicillin/clavulanic acid induced hepatotoxicity and the modulatory effect of gallic acid (GA)/ vitamin C (VTC) individually and in combination on oxidative stress-related liver damage. Sixty-four male albino rats were randomly separated into eight groups; negative control; GA group; VTC group; GA +VTC group; AC- treated group; AC + GA- treated group; AC + VTC treated group & AC+ GA + VTC treated group. A twice daily dose of AC (31.83 mg/kg) and a single daily dose of both GA (60 mg/kg) and VTC (200 mg/kg/day) were introduced to rats orally for 7 consecutive days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and tumor necrosis factor alpha (TNF-α) were significantly increased and upregulation of caspase-3 protein in rats treated with AC. Hepatic contents of malondialdehyde (MDA) were markedly increased following AC administration but produced a significant decrease in the levels of reduced glutathione (GSH) and glutathione-S-transferase (GST) along with downregulated the expression of the hemeoxygenase-1 gene (HMOX-1). These findings were in accordance with the histopathological findings. Co-administration of GA and/or VTC along with AC to rats reduced liver injury, oxidative stress, apoptosis and histopathological alterations. So, we concluded that GA and VTC pose a positive modulatory effect against AC induced hepatotoxicity.

Background & Aim Dyslipidaemia is highly prevalent among postmenopausal women and its management represents a keystone in the prevention of the worldwide increase in cardiovascular morbidity and mortality. Therapy choices for menopause-associated dyslipidaemia are limited and a matter of debate. So, it becomes prudent to search for natural safe alternatives. Vitamin D (VD) has been acknowledged as an essential factor in cardiovascular health. Thus, we aimed to illustrate the impact of different VD status on dyslipidaemia and atherogenic indices. Method 5 groups of rats were conducted; SHAM group fed control diet, ovariectomized rats fed control diet (OVX), ovariectomized rats fed VD-sufficient-high fat diet (HFD) (1 000 IU/ kg diet), ovariectomized rats fed VD-deficient-HFD (25 IU/ kg diet), and ovariectomized rats fed VD-replete-HFD (10 000 IU/ kg diet) for 16 weeks. Results Dyslipidaemia with an increased atherogenic index of plasma, atherosclerosis coefficient, cardiac risk ratio, and aortic total cholesterol accumulation in addition to reduced serum 25-hydroxy-VD levels was observed in the OVX and VD-sufficient HFD versus SHAM. These findings were aggravated by VD-deficient-HFD while reversed by VD-replete-HFD. The VD-mediated abundance of aortic ATP-binding cassette transporter A1 (ABCA1) expression, reduced activity of the inflammatory Jun N-terminal kinases (JNK), and downregulation of aortic cluster of differentiation-36 (CD36) receptors expression together with increased serum total antioxidant capacity and reduced serum malondialdehyde were among the supposed mechanisms. Conclusions Our study sheds light on alarming levels of VD deficiency among ovariectomized rats. VD repletion improved the menopause-associated dyslipidaemia and atherogenic indices through hypolipidemic, antioxidant, and anti-inflammatory effects.

Background: Reactive Oxygen Species (ROS) production has been established as an essential contributor in the development cardiotoxicity. The increase of ROS production simultaneously leads to the inhibition of anti-oxidant systems. Forkhead transcription factor O1 (FOXO1) plays an important role in regulating metabolism and oxidant stress. Clozapine was used to induce cardiotoxicity. Forskolin the well-known anti-oxidant and anti-inflammatory agent was used to modulate the effect on both FOXO1 gene and its target gene catalase and to what extent it may protect against clozapine-induced cardiotoxicity. Methods: The animals were classified into: control group, forskolin group; forskolin was administered for 8 weeks; clozapine group, and forskolin + clozapine group; forskolin was pre-administered for 5 weeks then continued along with clozapine for the last 3 weeks. RT-qPCR and gel electrophoresis were done. We analyzed the relation between FoxO1 gene and oxidative stress. Results: These effects are achieved by the ability of Forskolin to modulate the expression of Foxo-1 and catalase, the levels of CKMB, troponin I, GST, MDA, and TNF- α, Caspase-3 were decreased, histopathological changes were improved. Forskolin reduce cardiomyocytes damage, and improve cardiac function by decreasing oxidative stress. Conclusion: Forkolin with its biological activities and anti-oxidative effects control cardiotoxicity induced by ROS in addition to its anti-inflammatory activity. This may be considered as therapy in cardiac problems management.