Keratometric Outcomes after Simultaneous versus Sequential Intracorneal Ring Segment Implantation with Femtosecond Laser and Corneal Collagen Crosslinking in Egyptian Patients with Keratoconus and Ectasia.

Background: Keratoconus (KC) is degenerative corneal disorder, with central and paracentral thinning and corneal ectasia. For KC progressive cases, primary treatment included corneal collagen cross linking (CXL) to stabilize coning and intracorneal rings segment (ICRS) to correct visual acuity. Aim: The aim of the study is to assess efficacy and safety of ICRS and CXL on one session (Simultaneous) or two sessions (sequential) with maximum of 1 month apart. Patients and Methods: This Prospective Intervention Comparative research made at Armed forces hospital, Cairo, Egypt from January 2017 to December 2019. Forty patients (60 eyes) with mild to moderate KC were enrolled. Patients sorted into Simultaneous group includes 21 patients (30 eyes) undergo two procedures (ICRS then CXL) at the same session and Sequential group included 19 patients (30 eyes) undergo ICRS then CXL on two sessions with month apart. Patients followed up at end of 1st, 3rd, and 6th months. Assessment included changes in corrected corneal surface irregularities as minimum keratometric 1 (K1), maximum keratometric readings (K2), and mean keratometric (Km) readings. Results: Improvement of K1, K2, and Km in Simulations and Sequential groups achieved at end of 1st-, 3rd-, and 6th-month postoperative versus preoperative. Maximum improvement in Simulations and Sequential groups in K1 achieved at end of 6th and 1st months, in K2 at end of 3rd and 6th months and in Km at end of 1st and 3rd months. Conclusions: Combined ICRS and CXL act safely in one or two sessions and there are no statistically significant variations between results on both methods in keratometric readings.

Significance of Interleukin 23 in Systemic Lupus Patients: Relation to Disease Activity and Damage Indices.

Background: Dysregulation of both cellular and humoral immune responses is central in systemic lupus erythematosus (SLE) pathogenetic mechanisms. Proinflammatory cytokines, such as interleukin 23 (IL23), and their roles in promoting such dysregulation have recently been highly considered. This research compared IL23 serum levels in 85 Egyptian SLE patients and 85 healthy controls. Then, IL23 level was correlated to various SLE disease parameters, disease activity, and damage indices. Results: IL23 serum levels were significantly elevated in SLE patients versus healthy individuals. Furthermore, IL23 levels were positively correlated with SLE disease activity index (SLEDAI) and were positively correlated with arthritis, seizures, consumption of complements (C3, C4), and with parameters of nephritis (hematuria, pyuria, casts, and proteinuria). A positive correlation was also found between IL23 levels and oral prednisolone dose. Conclusion: IL23 has higher levels in the serum of SLE patients, and is correlated to activity of the disease, especially lupus nephritis. Further researchis needed to explore its exact role in SLE pathogenesis and whether it can be considered a potential biomarker or therapeutic target in SLE.

Identification and functional characterization of two rare LDLR stop gain variants (p.C231* and p.R744*) in Saudi familial hypercholesterolemia patients.

BACKGROUND: Familial hypercholesterolemia (FH) is a globally underdiagnosed inherited metabolic disorder. Owing to limited published data from Arab world, this study was conducted with the aim of identifying the genetic and molecular basis of FH in highly consanguineous Saudi population. METHODS: We performed clinical screening, biochemical profiling, whole exome sequencing and variant segregation analysis of two Saudi FH families. Additionally, 500 normolipic individuals were screened to ensure the absence of FH variant in general Saudi population. Functional characterization of FH variants on secondary structure characteristics of RNA and protein molecules was performed using different bioinformatics modelling approaches. RESULTS: WES analysis identified two independent rare LDLR gene stop gain variants (p.C231* and p.R744*) consistent to the clinical presentation of FH patients from two different families. RNAfold analysis has shown that both variants were predicted to disturb the free energy dynamics of LDLR mRNA molecule and destabilize its folding pattern and function. PSIPRED based structural modelling analysis has suggested that both variants bring drastic changes disturbing the secondary structural elements of LDLR molecule. The p.C231* and p.R744* variants are responsible for partial or no protein product, thus they are class 1 variants causing loss of function (LoF) LDLR variants. CONCLUSIONS: This study highlights the effectiveness of the WES, sanger sequencing, and computational analysis in expanding FH variant spectrum in culturally distinct populations like Saudi Arabia. Genetic testing of FH patients is very essential in better clinical diagnosis, screening, treatment, and management and prevention of cardiovascular disease burden in the society.

Colossolactone-G synergizes the anticancer properties of 5-fluorouracil and gemcitabine against colorectal cancer cells.

Several terpenoids were isolated from Ganoderma colossum with potential chemotherapeutic properties against different solid tumor cells. Herein, we further assessed the potential chemomodulatory effects of colossolactone-G to gemcitabine (GCB) and 5-fluorouracil (5-FU) against colorectal cancer cells. Colossolactone-G induced moderate cell killing effects against both HT-29 and HCT-116 cells, with IC50's of 90.5 ± 1.7 µM and 22.3 ± 3.9 µM, respectively. Equitoxic combination demonstrated a synergistic effect between colossolactone-G and GCB, or 5-FU with combination indices ranging from 0.22 to 0.67. Both GCB and 5-FU induced moderate cell cycle arrest at G0/G1-phase and S-phase. Despite colossolactone-G's lack of influence on cell cycle distribution, it significantly potentiated GCB- and 5-FU-induced cell cycle arrest. Similarly, colossolactone-G treatment alone did not induce pronounced apoptosis in both cell lines. However, 5-FU and GCB induced significant apoptosis which was further potentiated via combination with colossolactone-G. Furthermore, colossolactone-G significantly increased autophagic cell death response in both HCT-116 and HT-29 cells and potentiated 5-FU- and GCB-induced autophagic cell death. The influence of colossolactone-G alone or in combination with GCB or 5-FU on the apoptosis and autophagy were confirmed by qPCR analysis for the expression of several key apoptosis and autophagy genes such as, TRAIL, TP53INP1, BNIP3, hp62, ATG5, ATG7, Lamp2A and the golden standard for autophagy (LC3-II). In conclusion, a synergistic effect in terms of anticancer properties was observed when colossolactone-G was combined with 5-FU and GCB, where it influenced both apoptosis and autophagic cell death mechanisms.

Evaluation of irisin, retinol-binding protein 4, and leptin serum levels as biomarkers of macrovascular complications involvement in Saudi type 2 diabetes mellitus. A case-control study.

OBJECTIVES: To evaluate adipokine serum values of irisin, retinol-binding protein 4, and leptin in Saudi cases with type 2 diabetes mellitus (T2DM) for providing markers of T2DM macrovascular complications. Methods: This case-control research was carried out at Erfan Hospital, Jeddah, Saudi Arabia. The study included 138 subjects, classified into 3 groups: 46 T2DM patients with macrovascular complications, 46 T2DM without macrovascular complications, and 46 controls. Participants evaluated clinically and some biochemical parameters were measured. Results: Diabetic with and without macrovascular complications showed elevation of retinol-binding protein 4 (RBP4) and leptin; decreased irisin serum levels versus controls. Serum irisin was lower (p=0.007), while RBP4 was higher (p less than 0.0001) in T2DM patients with macrovascular complications versus without. Irisin showed negative correlations with fasting blood glucose (FBG), insulin, homeostatic model assessment of insulin resistance (HOMA-IR), RBP4, hemoglobin A1C (HbA1C), triglyceride, cholesterol, and low-density lipoprotein cholesterol. While RBP4 showed positive correlations with fasting blood glucose, insulin, HOMA-IR, leptin, and HbA1c; but a negative association with high-density lipoprotein cholesterol. Conclusion: Type 2 DM patients had raised RBP4 and leptin, but lower irisin levels versus controls. Irisin was lower, but RBP4 was higher in T2DM patients with macrovascular complications versus without, suggesting T2DM patients in pro-inflammatory conditions. These results suggested that irisin is protective, while RBP4 is a risk factor for T2DM macrovascular complications.

Thymoquinone Enhances Paclitaxel Anti-Breast Cancer Activity via Inhibiting Tumor-Associated Stem Cells Despite Apparent Mathematical Antagonism.

Thymoquinone (TQ) has shown substantial evidence for its anticancer effects. Using human breast cancer cells, we evaluated the chemomodulatory effect of TQ on paclitaxel (PTX). TQ showed weak cytotoxic properties against MCF-7 and T47D breast cancer cells with IC50 values of 64.93 ± 14 µM and 165 ± 2 µM, respectively. Combining TQ with PTX showed apparent antagonism, increasing the IC50 values of PTX from 0.2 ± 0.07 µM to 0.7 ± 0.01 µM and from 0.1 ± 0.01 µM to 0.15 ± 0.02 µM in MCF-7 and T47D cells, respectively. Combination index analysis showed antagonism in both cell lines with CI values of 4.6 and 1.6, respectively. However, resistance fractions to PTX within MCF-7 and T47D cells (42.3 ± 1.4% and 41.9 ± 1.1%, respectively) were completely depleted by combination with TQ. TQ minimally affected the cell cycle, with moderate accumulation of cells in the S-phase. However, a significant increase in Pre-G phase cells was observed due to PTX alone and PTX combination with TQ. To dissect this increase in the Pre-G phase, apoptosis, necrosis, and autophagy were assessed by flowcytometry. TQ significantly increased the percent of apoptotic/necrotic cell death in T47D cells after combination with paclitaxel. On the other hand, TQ significantly induced autophagy in MCF-7 cells. Furthermore, TQ was found to significantly decrease breast cancer-associated stem cell clone (CD44+/CD24-cell) in both MCF-7 and T47D cells. This was mirrored by the downregulation of TWIST-1 gene and overexpression of SNAIL-1 and SNAIL-2 genes. TQ therefore possesses potential chemomodulatory effects to PTX when studied in breast cancer cells via enhancing PTX induced cell death including autophagy. In addition, TQ depletes breast cancer-associated stem cells and sensitizes breast cancer cells to PTX killing effects.

Levels of soluble cell adhesion molecules in type 2 diabetes mellitus patients with macrovascular complications.

OBJECTIVE: Type 2 diabetes mellitus (T2DM) is a main risk factor for development of cardiovascular diseases (CVDs) and endothelial dysfunction. This study aimed to investigate serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), intercellular adhesion molecule 1 (sICAM-1), and endothelium selectin (sE-selectin) in T2DM patients with macrovascular complications. METHODS: A cross-sectional study of 21 controls, 30 T2DM patients without CVDs, and 30 T2DM patients with CVDs was conducted. Serum levels of soluble adhesion molecules including sVCAM-1, sICAM-1, and sE-selectin were determined using ELISA. RESULTS: Serum levels of sVCAM-1, sICAM-1, and sE-selectin were higher in T2DM patients than in controls. Levels of serum sVCAM-1 were higher in T2DM patients with CVDs compared with T2DM patients without CVDs. In T2DM patients with CVDs, significant positive associations were observed between sVCAM-1, sICAM-1, and sE-selectin levels (r = 0.575, p = 0.001 and r = 0.378, p = 0.040). CONCLUSIONS: Circulating levels of soluble adhesion molecules were elevated in T2DM patients, regardless of whether the patients had cardiovascular complications. Only sVCAM-1 was considered a useful marker for the prediction of CVDs in T2DM patients.

Liver ischemia/reperfusion injury, a setting in which the functional mass is reduced and the role of PDE5 inhibitor

Liver ischemia reperfusion is induced during surgical procedures like liver transplantation and resection. Multiple mechanisms have been postulated to liver damage following liver ischemia reperfusion injury, such as oxidative stress and inflammatory reactions. The present study declares the possible mechanism of tadalafil, toward modulating the inflammatory response. Forty-eight rats were divided into 4 groups as follows; Sham group subjected to midline laparotomy only. Tadalafil group administered Tadalafil 10 mg/kg intraperitoneal 45 min before sham operation. I/R (Ischemiareperfusion) group, rats undergo 60 min of hepatic ischemia followed by 60 min of reperfusion. Tadalafil + I/R group rats undergo a similar pattern of I/ R after the treatment with Tadalafil 10 mg/kg, 45 min before ischemia. At the end of the reperfusion, the blood samples were collected for estimation of biochemical markers including liver enzymes using colorimetric assay method and serum: TNF-α (tumor necrosis factor-α), IL-6 (interleukin 6) levels, ICAM- 1 (Intercellular Adhesion Molecule-1) were measured. Tissues were evaluated by semiquantitative and morphometrical approaches. Tadalafil succeeded in restoring normal levels of liver enzymes and ameliorating the oxidative stress as evidenced by decreasing MDA and restoring reduced glutathione levels in liver tissue homogenate. Also, Tadalafil exhibits anti-inflammatory effects, as it significantly decreased the levels of TNF-α, IL6 and ICAM-1. The findings are supported by BCL-2, TNF-α immunomarkers. It is concluded that modulation of the inflammatory response might be one of the mechanisms of Tadalafil-mediated hepatoprotection, so it is recommended as an adjuvant therapy in liver surgery

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Thymoquinone synergizes gemcitabine anti-breast cancer activity via modulating its apoptotic and autophagic activities.

The use of anti-cancer adjuvant therapy is rationalized by potentiating the efficacy, and/or protecting from major side effects of chemotherapeutics. Thymoquinone (TQ) is a naturally occurring compound with cumulative evidence of anti-cancer properties. In this study, we assessed the chemomodulatory potential of TQ to gemcitabine (GCB) against human breast adenocarcinoma (MCF-7), and ductal carcinoma (T47D) cells. TQ showed cytotoxic effects against MCF-7 and T47D with IC50's of 64.9 ± 14 µM and 165 ± 2 µM, respectively. The IC50's of GCB against MCF-7 and T47D were 0.9 ± 0.18 µM and 14.3 ± 2.8 µM and were significantly reduced after combination with TQ to 0.058 ± 12 µM and 2.3 ± 0.2 µM, respectively. The CI- values were indicative of synergism in MCF-7 and T47D cells (0.15 and 0.30, respectively). Further investigation showed that GCB caused significant anti-proliferative effect reflected by increasing cell population in S-phase in both cell lines. TQ potentiated GCB-induced anti-proliferative activity in both cell lines. GCB induced considerable apoptosis in T47D cell line, and TQ significantly increased GCB-induced apoptotic effects by 1.5 to 3.6 folds. Interestingly, GCB, TQ and their combination induced significant autophagic cell death in the apoptosis defected MCF-7 cells. In addition, TQ, GCB and their combination depleted breast cancer associated stem cell (CD44(+)/CD24(-)/(low)) clone within MCF-7 and T47D cells by 3.8% to 27.5%. In conclusion, TQ showed promising chemomodulatory effects to GCB against breast cancer cells via inducing apoptosis, necrosis and autophagy, in addition to depleting tumor associated resistant stem cell fraction.

Supplementation with Oligonol, Prevents Weight Gain and Improves Lipid Profile in Overweight and Obese Saudi Females.

BACKGROUND: Obesity is a global health problem, increasing susceptibility to Type 2 Diabetes (T2DM) and Cardiovascular Disease (CVD). Varieties of products have been proposed for treatment with varying degrees of success. Recent studies, suggested Oligonol; an optimized phenolic product mixture from Lychee Fruit Polyphenols (LFP); as such treatment in Japanese population. OBJECTIVES: We aimed to investigate the effect of oligonol on weight, insulin resistance by (HOMA-IR), lipids profile, leptin, Adiponectin, and resistin in healthy overweight and obese Saudi females. SUBJECTS AND METHODS: 60 Saudi healthy overweight and obese females were enrolled in a double blind case/control study to take either Oligonol or placebo for 12 weeks without dietary or lifestyle re-strictions. Weight, height, Waist Circumference (WC), hip circumference (HC), and blood pressure were measured, and fasting blood samples of participants were taken before, and at the end of study. Total cholesterol, HDL-cholesterol, triglycerides, glucose, insulin, leptin, adiponectin, and resistin were meas-ured. LDL- cholesterol, HOMA-IR were calculated by equation. RESULTS: 47 subjects completed the study, 25 in placebo group, and 22 in Oligonol group. No ill effects were noted in any participant. Oligonol reduced means of serum triglycerides (P=0.008), and resistin (P=0.045) significantly. In addition, no weight gain was noted in oligonol group, unlike placebo group which exhibited significant increase in mean weight (P= 0.036), WC (P=0.027), HC (P= 0.047), and leptin (P <0.001). CONCLUSION: Oligonol could be suggested as future hypolipidemic and weight controlling agent for overweight and obese Saudi females.

Protective role of CoQ10 or L-carnitine on the integrity of the myocardium in doxorubicin induced toxicity.

Doxorubicin (DOX) is a chemotherapeutic agent used for treatment of different cancers and its clinical usage is hindered by the oxidative injury-related cardiotoxicity. This work aims to declare if the harmful effects of DOX on heart can be alleviated with the use of Coenzyme Q10 (CoQ10) or L-carnitine. The study was performed on seventy two female Wistar albino rats divided into six groups, 12 animals each: Control group; DOX group (10mg/kg); CoQ10 group (200mg/kg); L-carnitine group (100mg/kg); DOX+CoQ10 group; DOX+L-carnitine group. CoQ10 and L-carnitine treatment orally started 5days before a single dose of 10mg/kg DOX that injected intraperitoneally (IP) then the treatment continued for 10days. At the end of the study, serum biochemical parameters of cardiac damage, oxidative stress indices, and histopathological changes were investigated. CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 ß), tumor necrosis factor alpha (TNF-α), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels. Both corrected the cardiac alterations histologically and ultrastructurally. With a visible improvements in α-SMA, vimentin and eNOS immunohistochemical markers. CoQ10 or L-carnitine supplementation improves the functional and structural integrity of the myocardium.

Methylene tetrahydrofolate reductase, transforming growth factor-ß1 and lymphotoxin-α genes polymorphisms and susceptibility to rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis is a widely prevalent autoimmune disorder with suggested genetic predisposition. OBJECTIVES: The aim of this study is to detect the pattern of genetic polymorphism of methylene tetrahydrofolate reductase (MTHFR C677 T and A1298 C), transforming growth factor-ß1 (TGF-ß1 T869 C) and lymphotoxin-α (LT-α A252G) in patients having rheumatoid arthritis and correlate these patterns to disease activity and serum levels of tumor necrosis factor-alpha (TNF-α), B-Cell Activating Factor (BAFF), and osteopontin. METHODS: A total of 194 subjects, 90 controls and 104 patients with rheumatoid arthritis were genotyped for MTHFR C677 T and A1298 C, TGF-ß1 T869 C and LT-α A252G polymorphisms using a methodology based on PCR-RFLP. Also serum levels of TNF-α, osteopontin and BAFF were measured by ELISA kits. RESULTS: The CT genotype and T allele of MTHFR C677 T and GG genotype and G allele of LT-α A252G are associated with the risk of RA and with higher levels of the pro-inflammatory cytokine, TNF-α in patients with rheumatoid arthritis. CONCLUSION: Our findings suggest that there is association between MTHFR C677 T and LT-α A252G genes polymorphisms and increased risk of RA in this sample of Egyptian population.

Methylene tetrahydrofolate reductase, transforming growth factor-ß1 and lymphotoxin-α genes polymorphisms and susceptibility to rheumatoid arthritis / Polimorfismos dos genes metilenotetrahidrofolato redutase, fator de crescimento transformador β1 e linfotoxina-α e susceptibilidade à artrite reumatoide

ABSTRACT Background: Rheumatoid arthritis is a widely prevalent autoimmune disorder with suggested genetic predisposition. Objectives: The aim of this study is to detect the pattern of genetic polymorphism of methylene tetrahydrofolate reductase (MTHFR C677 T and A1298 C), transforming growth factor-β1 (TGF-β1 T869 C) and lymphotoxin-α (LT-α A252G) in patients having rheumatoid arthritis and correlate these patterns to disease activity and serum levels of tumor necrosis factor-alpha (TNF-α), B-Cell Activating Factor (BAFF), and osteopontin. Methods: A total of 194 subjects, 90 controls and 104 patients with rheumatoid arthritis were genotyped for MTHFR C677 T and A1298 C, TGF-β1 T869 C and LT-α A252G polymorphisms using a methodology based on PCR-RFLP. Also serum levels of TNF-α, osteopontin and BAFF were measured by ELISA kits. Results: The CT genotype and T allele of MTHFR C677 T and GG genotype and G allele of LT-α A252G are associated with the risk of RA and with higher levels of the pro-inflammatory cytokine, TNF-α in patients with rheumatoid arthritis. Conclusion: Our findings suggest that there is association between MTHFR C677 T and LT-α A252G genes polymorphisms and increased risk of RA in this sample of Egyptian population.

RESUMO Antecedentes: A artrite reumatoide é uma doença autoimune amplamente prevalente com sugerida predisposição genética. Objetivos: Detectar o padrão de polimorfismo dos genes metilenotetrahidrofolato redutase (MTHFR C677 T e A1298 C), fator de crescimento transformador β1 (TGF-β1 T869 C) e linfotoxina-α (LT-α A252G) em pacientes com artrite reumatoide e correlacionar esses padrões com a atividade da doença e os níveis séricos de fator de necrose tumoral alfa (TNF-α), fator ativador de linfócitos B (BAFF) e osteopontina. Métodos: Foram genotipados 194 indivíduos – 90 controles e 104 com artrite reumatoide – à procura de polimorfismos dos genes MTHFR C677 T e A1298 C, TGF-β1 T869 C e LT-α A252G com uma metodologia baseada na PCR-RFLP. Mensuraram-se também os níveis séricos de TNF-α, osteopontina e BAFF com kits de Elisa. Resultados: O genótipo CT e o alelo T do MTHFR C677 T e o genótipo GG e alelo G do LT-α A252G estão associados ao risco de AR e a níveis mais elevados da citocina pró-inflamatória TNF-α em pacientes com artrite reumatoide. Conclusão Os achados do presente estudo sugerem que há associação entre os polimorfismos dos genes MTHFR C677 T e LT-α A252G e um risco aumentado de AR nessa amostra da população egípcia.

Prophylactic role of coenzyme Q10 and Cynara scolymus L on doxorubicin-induced toxicity in rats: Biochemical and immunohistochemical study.

OBJECTIVE: The study aims to evaluate the protective effects of coenzyme Q10 (CoQ10) and Cynara scolymus L (CS) on doxorubicin (dox)-induced toxicity. MATERIALS AND METHODS: Sixty male rats were divided into six groups. Group 1 as a control. Group 2 received dox (10 mg/kg) intraperitoneally. Group 3 received CoQ10 (200 mg/kg). Group 4 received CS (500 mg/kg). Group 5 received CoQ10 (200 mg/kg) and dox (10 mg/kg). Group 6 received CS (500 mg/kg) and dox (10 mg/kg). The rats were then evaluated biochemically and immunohistochemically. RESULTS: Dox produced a significant deterioration of hepatic and renal functional parameters. Moreover, an upsurge of oxidative stress and nitrosative stress markers. The expression of alpha-smooth muscle actin (α-SMA) was increased and proliferating cell nuclear antigen (PCNA) expression was decreased. Administration of CoQ10 and CS resulted in a significant improvement of hepatic and renal functional parameters, and an improvement of both α-SMA and PCNA. CONCLUSION: It is concluded that pretreatment with CoQ10 and CS is associated with up-regulation of favorable protective enzymes and down-regulation of oxidative stress. That can be advised as a supplement to dox-treated patients.

The role of Acacia Arabica extract as an antidiabetic, antihyperlipidemic, and antioxidant in streptozotocin-induced diabetic rats.

OBJECTIVE: To investigate the role of Acacia Arabica extract as a hypoglycemic, antihyperlipidemic, and antioxidant agent in streptozotocin-induced diabetic rats. METHODS: This is an animal experimental study conducted in King Fahd Research Center, King Abdulaziz University (KAU), Jeddah, Kingdom of Saudi Arabia from December 2012 to January 2013. Thirty-six female albino rats were divided into 2 equal groups; the first served as control, and the second was the streptozotocin-induced diabetic group. Each group was subdivided into 3 subgroups, each of 6 rats; the first was left untreated, the second and the third were treated with Acacia Arabica extract orally for 21 days (100 mg/kg for the second group and 200 mg/kg for the third group). On the twenty-first day, blood samples were withdrawn through the retro-orbital plexus of overnight fasted rats under light ether anesthesia for determination of serum glucose, insulin, total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), malondialdehyde (MDA), and coenzyme Q10 (Co-Q10). RESULTS: A significant decrease in levels of serum glucose, insulin resistance, TC, TG, LDL-C, MDA and a significant increase in HDL-C and Co-Q10 was observed in the treated diabetic groups when compared to the untreated diabetic group. The changes were dose dependent. CONCLUSION: The results found in this study indicate that Acacia Arabica extract has hypoglycemic, hypolipidemic, and antioxidant properties, therefore, it can be investigated for its efficacy in the treatment of diabetes in humans.

Protective role of antioxidants on thioacetamide-induced acute hepatic encephalopathy: biochemical and ultrastructural study.

Thioacetamide (TAA) has been used in development of animal models of acute hepatic encephalopathy (AHE). This experimental study was designed to evaluate effects of oral administration of vitamin C, vitamin E and their combination on liver and brain enzymes and their histologic and ultrastructure changes. Eighty Wistar rats were included and divided into five groups (16 each). Group 1 (control) received saline once intraperitoneally (IP) then administered orally saline and corn oil for 3 days. Group 2 [hepatotoxic (TAA)] were received TAA (300mg/kg) once intraperitoneally (IP). Group 3 (vitamin C and TAA) received TAA (300mg/kg) once intraperitoneally (IP) and then administered orally vitamin C (100mg/kg) daily for 3 days. Group 4 (vitamin E and TAA) received TAA (300mg/kg) once intraperitoneally (IP) and then administered orally vitamin E (200mg/kg) daily for 3 days. Group 5 (vitamin C and vitamin E and TAA) received TAA (300mg/kg) once intraperitoneally (IP) and then administered orally vitamin C (100mg/kg) in combination with vitamin E (200mg/kg) daily for 3 days. All rats were sacrificed 24h after last treatment under anesthesia. Blood samples were collected and serum was obtained for analysis of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), total protein, triglyceride, cholesterol using spectrophotometer and ELISA kits. Liver and brain were extracted and tissue homogenate was used to measure malondialdehyde (MDA), reduced glutathione (GSH) and nitric oxide (NO). Histological and ultrastructure examination were done. TAA induced significant increase of MDA and decreased in GSH and NO in both liver and brain homogenate with more liver affection, and increased in serum levels of AST, ALT, triglyceride, cholesterol and decreased in total protein. Furthermore, there is decrease in serum levels of AST, ALT, triglyceride, cholesterol and tissue levels of MDA and elevated serum total protein and tissue GSH and NO under the umbrella of vitamin C and vitamin E and their combination, although vitamin E is more efficient. These data showed protective effect of vitamins C and E, especially vitamin E against oxidative stress and hepatic and brain damage, and histological architecture of the liver in rats' model of acute hepatic encephalopathy elicited by TAA.