L-Arginine-induced acute pancreatitis and its associated lung injury in rats: Down-regulation of TLR-4/MAPK-p38/JNK signaling pathway via Ginkgo biloba extract EGb 761.

Objectives: Acute pancreatitis (AP) is an abrupt inflammatory condition characterized by a storm of inflammatory cytokines leading to high morbidity and mortality. The current study aimed to examine the efficacy of Ginkgo biloba extract EGb 761 (GBE) in the treatment of L-arginine-induced AP and its associated lung injury. Materials and Methods: Forty rats were randomly assigned into four groups. The normal group received only saline intraperitoneally while the other groups received two intraperitoneal L-arginine injections (250 mg/100 g b.wt) separated by a 1-hour interval to provoke AP. GBE (200 and 400 mg/kg/day, PO) was administered for 2 weeks post-induction of pancreatitis. Sera and pancreatic tissues were isolated. Results: The outcome of the present study revealed that GBE ameliorated the elevated levels of serum amylase, lipase, and pancreatic inflammatory mediators viz., tumor necrosis factor-alpha (TNF-α), mitogen-activated protein kinase P38 (MAPK-P38), c-Jun N-terminal kinase 1 (JNK1), and nuclear factor-kappa B (NF-κB). Moreover, GBE restored the pancreatic gene expression of Toll-like receptor 4 (TLR4) and prostatic acid phosphatase-2 (PAP-2). Pancreatic and lung histopathological examinations confirmed the aforementioned parameters. Conclusion: GBE interfered with the mechanistic pathway of L-arginine-induced acute pancreatic and its associated lung injury. Due to its anti-inflammatory properties, GBE can be used as a novel therapeutic candidate for the treatment of AP through down-regulating TLR-4/MAPK-p38/JNK and MAPK- p38/NF-κB signaling cascades.

Fisetin mitigates letrozole-induced polycystic ovarian syndrome in rats: crosstalk of AMPK/PI3K/AKT-mediated-Nrf2 antioxidant defense mechanism and the inflammasome NLRP3/NF-κB P65/IL-1ß signaling pathways.

Polycystic ovarian syndrome (PCOS) is a highly prevalent condition affecting reproductive-aged women, causing insulin resistance, hyperandrogenism, weight gain, and menstrual problems. The present study intended to investigate the potential role of fisetin (FT) in letrozole (LZ)-induced PCOS in adult female rats and the possible mechanism underlying its action. PCOS was induced by oral administration of LZ (1 mg/kg) for 21 days. Treated rats received FT (1.25 or 2.5 mg/kg) orally once daily for 14 consecutive days. Following the experimental duration, blood samples and ovary tissues were isolated and preserved for biochemical and histopathological examinations. The results revealed that LZ-induced PCOS led to significant abnormalities in sex hormones and metabolic parameters. Additionally, it initiated an inflammatory cascade, evidenced by activation of the NF-κB p65/IL-1ß and AMPK/PI3K/AKT pathways, alongside downregulation of Nrf2 ovarian gene expression and NLRP3 inflammasome activity, which enhanced the production of proinflammatory cytokines. FT demonstrated its beneficial impacts by restoring hormonal disturbance and reversing the imbalanced metabolic parameters. Moreover, FT increased the mRNA of ovarian Nrf2 levels and suppressed the up-regulated inflammatory IL-1ß/NF-κB p65 signaling pathway, consequently alleviating the elevated levels of ovarian NLRP3. The histopathological examination also confirmed that FT has a beneficial effect in ameliorating PCOS, consistent with the aforementioned parameters. Finally, the present results demonstrated that FT ameliorates LZ-induced PCOS through the intricate interplay between the AMPK/PI3K/AKT-mediated Nrf2 antioxidant defense mechanism and the regulation of the inflammasome NLRP3/NF-κB p65/IL-1ß signaling pathways.

The relation between autophagy modulation by intermittent fasting and aquaporin 2 expression in experimentally induced diabetic nephropathy in albino rat.

Polyuria is an early sign of diabetic nephropathy (DN) that produces dehydration in diabetic patients. This could be caused by alteration of renal aquaporin 2 (AQP2) expression. This study aimed to describe the relation between autophagy modulation via intermittent fasting (IF) and renal AQP2 expression and polyuria in case of DN. We divided the rats into control, DN and IF groups. After 2 and 4 weeks of diabetes induction, blood glucose (BG), serum creatinine (Scr), urine volume, and 24 hours urine protein (UP) were examined. Diabetic nephropathy histopathological index (DNHI) was calculated to evaluate histopathological changes. Immunohistochemistry and real-time PCR were performed to measure the levels of AQP2 and the autophagy marker; LC3 in kidney tissue. DNHI was correlated to the PCR and immunoexpression of AQP2 and LC3. Intermittent fasting significantly decreased the BG, Scr, urine volume, 24 hours UP, and DNHI as compared diabetes. Diabetes significantly elevated the immunoreactivity and mRNA expression levels of AQP2 and LC3 as compared to the control. However, the IF decreased AQP2 and stimulated autophagy in cyclic fashion. Our data revealed significant positive correlations between AQP2 and LC3 at the level of immunoexpression and mRNA at 2nd weeks. Taken together, these data showed that autophagy stimulation didn't regulate AQP2 expression in case of diabetic nephropathy, however IF decreased polyuria through improvement of glycemic state.

Novel drugs affecting diabetic peripheral neuropathy.

Diabetic peripheral neuropathy (DPN) poses a significant threat, affecting half of the global diabetic population and leading to severe complications, including pain, impaired mobility, and potential amputation. The delayed manifestation of diabetic neuropathy (DN) makes early diagnosis challenging, contributing to its debilitating impact on individuals with diabetes mellitus (DM). This review examines the multifaceted nature of DPN, focusing on the intricate interplay between oxidative stress, metabolic pathways, and the resulting neuronal damage. It delves into the challenges of diagnosing DN, emphasizing the critical role played by hyperglycemia in triggering these cascading effects. Furthermore, the study explores the limitations of current neuropathic pain drugs, prompting an investigation into a myriad of pharmaceutical agents tested in both human and animal trials over the past decade. The methodology scrutinizes these agents for their potential to provide symptomatic relief for DPN. The investigation reveals promising results from various pharmaceutical agents tested for DPN relief, showcasing their efficacy in ameliorating symptoms. However, a notable gap persists in addressing the underlying problem of DPN. The results underscore the complexity of DPN and the challenges in developing therapies that go beyond symptomatic relief. Despite advancements in treating DPN symptoms, there remains a scarcity of options addressing the underlying problem. This review consolidates the state-of-the-art drugs designed to combat DPN, highlighting their efficacy in alleviating symptoms. Additionally, it emphasizes the need for a deeper understanding of the diverse processes and pathways involved in DPN pathogenesis.

Eugenol alleviates acrylamide-induced rat testicular toxicity by modulating AMPK/p-AKT/mTOR signaling pathway and blood-testis barrier remodeling.

This study aimed to investigate the effects of eugenol treatment on reproductive parameters in acrylamide (ACR)-intoxicated rats. The study evaluated alterations in relative testes and epididymides weights, sperm quality, serum hormonal status, seminal plasma amino acids, testicular cell energy and phospholipids content, oxidative and nitrosative stress parameters, adenosine monophosphate-activated protein kinase/ phosphoinositide 3-kinase/phosphor-protein kinase B/mammalian target of rapamycin (AMPK/PI3K/p-AKT/mTOR) signaling pathway, blood-testis barrier (BTB) remodeling markers, testicular autophagy and apoptotic markers, as well as histopathological alterations in testicular tissues. The results revealed that eugenol treatment demonstrated a significant improvement in sperm quality parameters, with increased sperm cell concentration, progressive motility live sperm, and a reduction in abnormal sperm, compared to the ACR-intoxicated group. Furthermore, eugenol administration increased the levels of seminal plasma amino acids in a dose-dependent manner. In addition, eugenol treatment dose-dependently improved testicular oxidative/nitrosative stress biomarkers by increasing oxidized and reduced glutathione levels and reducing malondialdehyde and nitric oxide contents as compared to ACRgroup. However, eugenol treatment at a high dose restored the expression of AMPK, PI3K, and mTOR genes, to levels comparable to the control group, while significantly increasing p-AKT content compared to the ACRgroup. In conclusion, the obtained findings suggest the potential of eugenol as a therapeutic agent in mitigating ACR-induced detrimental effects on the male reproductive system via amelioration of ROS-mediated autophagy, apoptosis, AMPK/p-AKT/mTOR signaling pathways and BTB remodeling.

Pylorus ligation-induced hyperacidity: synergistic prophylactic effects of linagliptin and L-arginine via up-regulation of EP4 receptor subtype and improvement of vascular endothelial damage.

Gastric hyperacidity and ulceration are chronic diseases characterized by repeated healing followed by re-exacerbation. The study aims to protect against gastric hyperacidity without interfering with gastric acid secretion. Pylorus ligation-induced hyperacidity is commonly utilized in the induction of gastric ulcers.Forty-two rats were distributed into seven groups (n = 6). Group I comprised sham-operated group. Group II served as pylorus-ligation group. Groups III-VII were given oral Linagliptin (LN; 3 and 6 mg/kg), L-arginine (LA; 150 and 300 mg/kg) and their combination (LN 3 + LA 150 mg/kg), respectively for 7 days. On the 8th day, groups II-VII were subjected to pylorus-ligation.Treatment of pylorus-ligated rats with LN, LA and their combination improved the gastric hyperacidity as exhibited by a marked reduction in the gastric juice volume, total and free acidities and pepsin contents with a noticeable increase in pH. Pre-treatment with LN, LA and their combination showed a marked alleviation in the gastric inflammatory indicators evidenced by reduction in the gastric levels of MCP-1and Il-1ß as well as elevation of eNOS levels versus the sham-operated group. A marked up-regulation in the gastric gene expression of PGE, EP4 and VEGF accompanied by an improvement of the histopathologic pictures/scores, and TNF-α and caspase-3 immuno-staining were also recorded.By estimating the combination-index, it can be concluded that combining LN with LA exhibited prophylactic synergistic effects in ameliorating pylorus ligated-induced hyperacidity, mainly via up-regulation of EP4 receptor and improvement of vascular endothelial damage through VEGF expression in gastric mucosa.

Neuromodulatory role of L-arginine: nitric oxide precursor against thioacetamide-induced-hepatic encephalopathy in rats via downregulation of NF-κB-mediated apoptosis.

The aim of the present study was to investigate the impact of arginine (ARG), a nitric oxide (NO) precursor, on thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats by injection of TAA (100 mg/kg, i.p) three times per week for six consecutive weeks. TAA-injected rats were administered ARG (100 mg/kg; p.o.) concurrently with TAA for the six consecutive weeks. Blood samples were withdrawn, and rats were sacrificed; liver and brain tissues were isolated. Results of the present study demonstrated that ARG administration to TAA-injected rats revealed a restoration in the serum and brain ammonia levels as well as serum aspartate transaminase, alanine transaminase, and alkaline phosphatase and total bilirubin levels as well as behavioral alterations evidenced by restoration in locomotor activity, motor skill performance, and memory impairment. ARG showed also improvement in the hepatic and neuro-biochemical values, pro-inflammatory cytokines, and oxidative stress biomarkers. All these results were confirmed by histopathological evaluation as well as ultrastructural imaging of the cerebellum using a transmission electron microscope. Furthermore, treatment with ARG could ameliorate the immunological reactivity of nuclear factor erythroid-2-related factor 2 (Nrf2) and cleaved caspase-3 proteins in the cerebellum and hepatic tissues. From all the previous results, it can be fulfilled that ARG showed a beneficial role in modulating the adverse complications associated with TAA-induced HE in rats via reducing hyperammonemia and downregulating nuclear factor kappa B (NF-κB)-mediated apoptosis.

Uro-protective role of chrysin against cyclophosphamide-induced hemorrhagic cystitis in rats involving the turning-off NF-κB/P38-MAPK, NO/PARP-1 and STAT-3 signaling cascades.

BACKGROUND: Chemotherapeutic agents are used to treat a wide range of cancer types, but they cause serious side effects which must be managed after treatment. Cyclophosphamide (CYP) is one of chemotherapeutic drugs that causes hemorrhagic cystitis (HC) induced by acrolein. OBJECTIVE: The current investigation intended to uncover the role of chrysin (CHR) in CYP-induced HC in rats and explore the signaling pathway beyond this effect. ANALYSIS: process: A single dose of CYP (200 mg/kg/IP) was injected, meanwhile CHR (25, 50 and 100 mg/kg, P.O) was administered respectively for 7 days prior to CYP administration and resume for 7 days afterwards. Urinary bladder tissue was then isolated from all rats to assess oxidative stress and inflammatory biomarkers. Moreover, histopathological examinations were performed. RESULTS: Treatment with CHR showed a marked alleviation in oxidative stress biomarkers induced by CYP. Furthermore, CHR treatment presented a dose-dependent boost in the anti-inflammatory; IL-10 levels and a drop in the pro-inflammatory biomarkers; IL-1ß, IL-6, and TNF-α. Additionally, stabilization of the PARP-1 protein expression was also detected thus preventing DNA damage. Similarly, CHR restored the urinary bladder cGMP levels. Notably, CHR treatment was accompanied with inhibition in NF-κB/p38-MAPK, NO/PARP-1 and STAT-3 signaling pathways inflammatory cascades. All these findings conformed with the histopathological examinations as well as iNOS immunostaining in the urinary bladder tissue. CONCLUSION: Co-administration of CHR and CYP attained uro-protective therapeutic potential to guard against HC as well as spot the tangled mechanism of CHR in attenuating the HC induced by CYP.

The Reversed Flow Hemisoleus Propeller Muscle Flap.

BACKGROUND: Soleus muscle flap can be used in different modifications to reconstruct lower limb defects. It can be proximally based, distally based, island or reversed flow flap. The first description of the soleus muscle as an island flap supplied by one distal perforator was reported by Yajima et al (Plast Reconstr Surg. 1995;96:1162-1168). However, its use as a propeller flap supplied by the distal perforators and rotated for more than 90 degrees was not described yet. OBEJECTIVES: The aims of the study are to study the detailed vascular anatomy of the distal perforators of the soleus muscle flap and to demonstrate the applicability of using it as a propeller flap. PATIENTS AND METHODS: A total number of 42 patients were included in this study. These patients had various distal leg and foot defects. All patients were assessed preoperatively by Doppler study and computed tomography angiography to define the vascular status of the leg. The muscle was raised as a reversed flow flap, based on 1 or more distal perforators and its feeding vessel (posterior tibial artery) after being dissected and divided proximally. The muscle was rotated for more than 90 degrees to reach distal leg defects and approximately 180 degrees to reach the foot defects. RESULTS: All flaps survived completely with good and durable coverage. The vascularity of the limb was not affected in all patients. There was no functional donor site morbidity. CONCLUSIONS: The reversed flow hemisoleus muscle flap supplied by the distal perforators and the posterior tibial artery has a great arc of rotation that can cover all distal leg, ankle, and foot defects. Therefore, it can be used as alternative to free flap in lower extremity reconstruction. A new nomenclature is suggested for this flap which is the propeller hemisoleus muscle flap.

Doxorubicin-induced hepatic toxicity in rats: Mechanistic protective role of Omega-3 fatty acids through Nrf2/HO-1 activation and PI3K/Akt/GSK-3ß axis modulation.

Doxorubicin (DOX), a common antibiotic used to treat a variety of tumors, has several substantial adverse effects that limit its clinical use. As a result, finding effective protective agents to combat DOX-induced organ damage is a necessity. The current study was set to delineate the hepatoprotective role of omega-3 fatty acids (ω-3FA) against DOX-mediated acute liver damage in rats and the underlined mechanism of GSK-3ß inhibition. Five groups of rats were orally received either saline (groups 1 & 2) or ω-3FA (25, 50 and 100 mg/kg/day; groups 3, 4 & 5, respectively) for 28 consecutive days. Single DOX intraperitoneal injection (20 mg/kg) was used to induce hepatic toxicity in all groups except group 1 (negative control). Blood samples and liver tissues were collected 48-hr after injection. Our results revealed that pre-administration of ω-3FA (25, 50 and 100 mg/kg) to DOX-induced hepatic injured rats showed a significant reduction in serum hepatic injury biomarkers (ALT, AST, total and direct bilirubin) as well as hepatic contents of MDA, GSH, Nrf2 and HO-1. Additionally, hepatic PI3K, pAkt and GSK-3ß have been restored significantly in a dose-dependent manner. Furthermore, all the hepatic histopathological features have been retained upon ω-3FA treatment together with the immunostaining intensity of tumor necrosis factor-α and caspase-3. These results suggest that ω-3FA have shown a marked activation of the Nrf2/HO-1 signaling pathway and modulation of the PI3K/pAkt/GSK-3ß axis against DOX-induced hepatotoxicity.

Phytochemical profiling and anti-fibrotic activities of Plumbago indica L. and Plumbago auriculata Lam. in thioacetamide-induced liver fibrosis in rats.

This study aimed at investigating the chemical composition and the hepatoprotective activities of Plumbago indica L. and P. auriculata Lam. LC-MS/MS analyses for the hydroalcoholic extracts of the aerial parts of the two Plumbago species allowed the tentative identification of thirty and twenty-five compounds from P. indica and P. auriculata, respectively. The biochemical and histopathological alterations associated with thioacetamide (TAA)-induced liver fibrosis in rats were evaluated in vivo where rats received the two extracts at three different dose levels (100, 200 and 400 mg/kg p.o, daily) for 15 consecutive days with induction of hepatotoxicity by TAA (200 mg/kg/day, i.p.) at 14th and 15th days. Results of the present study showed a significant restoration in liver function biomarkers viz. alanine transaminase (ALT), aspartate transaminase (AST), gamma glutamyl transferase and total bilirubin. The liver homogenates exhibited increased levels of antioxidant biomarkers: reduced glutathione (GSH) and catalase (CAT), accompanied with decline in malondialdehyde (MDA). Furthermore, treated groups exhibited a significant suppression in liver inflammatory cytokines: tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6), and fibrotic biomarker: alpha smooth muscle relaxant. Histopathological examination of the liver showed normality of hepatocytes. Noteworthy, P. indica extract showed better hepatoprotective activity than P. auriculata, particularly at 200 mg/kg. To sum up, all these results indicated the hepatoprotective properties of both extracts, as well as their antifibrotic effect was evidenced by reduction in hepatic collagen deposition. However, additional experiments are required to isolate their individual secondary metabolites, assess the toxicity of the extracts and explore the involved mechanism of action.

Role of olmesartan in ameliorating diabetic nephropathy in rats by targeting the AGE/PKC, TLR4/P38-MAPK and SIRT-1 autophagic signaling pathways.

Diabetic nephropathy (DN) is one of the most serious consequences of diabetes and the most common reason for end-stage renal disease. The current study was set out to investigate the ability of olmesartan medoxomil (OM) to treat DN by evaluating the reno-protective effects of this drug on fat/fructose/streptozotocin (F/Fr/STZ)-induced diabetic rat model. This model was induced by feeding rats high F/Fr diet for 7 weeks followed by injection of a single sub-diabetogenic dose of STZ (35mg/kg; i.p). The F/Fr/STZ-induced diabetic rats were orally treated with either OM (10 mg/kg) or pioglitazone (10 mg/kg); as a standard drug daily for four consecutive weeks. F/Fr/STZ-induced diabetic rats propagated inflammatory, oxidative, and fibrotic events. OM was able to oppose the injurious effects of diabetes; it significantly reduced the elevated levels of advanced glycated end products (AGEs) and downregulated PKC gene expression, therefore, indicating its antioxidant capacity evidenced by mitigation in GSH, MDA renal content. Moreover, OM impaired the inflammatory cascade by suppressing the elevated level of renal TLR4 as well as diminished the inflammatory profibrotic cytokine TGF-ß1. Additionally, OM was able to turn off the MAPK cascade mediated by an upsurge in renal angiotensin 1-7 content and decrease the level of renal tubular injury marker, KIM-1. Furthermore, OM enhanced the autophagic activity pathway by upregulating of gene expression of SIRT-1. The histopathological examination confirmed these results. Finally, OM protected against type 2 diabetes-related nephropathy complications by altering inflammatory pathways, oxidative, fibrotic, and autophagic processes triggered by renal glucose overload. This study shows that OM has a reno-protective effect against DN in rats by inhibiting the AGE/PKC, TLR4/P38-MAPK, and SIRT-1 autophagic signaling pathways.

Telmisartan: An angiotensin receptor blocker regulates osteoclastogenesis via inhibition of the ERK triggering in osteoporotic male rats.

Great attention was recently given to the importance of RAS in controlling inflammatory bone diseases, following the discovery of its local existence in skeletal tissues. Local RAS was found to be expressed on osteoblastic and osteoclastic cells and to exert its action via angiotensin II (AngII) receptors, including angiotensin II type 1 receptor (AT1 R) and angiotensin II type 2 receptors. Telmisartan (TLM), an AT1 R blocker (ARBs), was investigated in the present study for its therapeutic effect on bone health in osteoporotic rats. d-Galactose, a reducing sugar at a dose of 200 mg/kg/day/i.p., was used to induce osteoporosis in male rats. TLM, at a dose of 5 mg/kg/day, was orally introduced in the osteoporotic rats for four consecutive weeks. Tibia and femur bone densitometry was estimated, bone formation and bone resorption biomarkers serum levels were measured, mineral content in blood was also valued, and finally the extracellular regulated kinase (ERK) expression in bone was determined. TLM considerably improved the deleterious effect of d-galactose on bone mineral density. It blunted serum bone-specific alkaline phosphatase and osteocalcin while elevating serum osteoprotegrin (OPG). On the other hand, TLM turned off the pronounced elevation in serum receptor activator of nuclear factor-κß ligand (RANKL), tartrate-resistant acid phosphatase, and cathepsin K. Furthermore, it significantly hindered the bone expression of ERK which hampered osteoclastogenesis. AT1 R inhibition abolished the rise in serum calcium and phosphorus and normalized serum superoxide dismutase and catalase. These TLM protective effects in d-galactose-treated rats were confirmed by the histopathological examination. The results all together denote the potential therapeutic value of ARBs therapy in osteoporosis.

Curcumin nanoemulsion ameliorates brain injury in diabetic rats.

Diabetes mellitus has been implicated in the exacerbation of cerebral ischemic injuries. Among the most promising therapeutic approaches is the combination of nutraceuticals and nanotechnology. Curcumin has been termed "the magic molecule", and it was proven to exert several therapeutic actions. Therefore, the aim of the presented work was to investigate the therapeutic effects of curcumin nanoemulsion (NC) administered orally on the middle cerebral artery occlusion and reperfusion (MCAO/Re)-induced cerebral damage in rats with streptozotocin-induced diabetes. The cerebral injury was induced in rats by MCAO/Re 6 weeks after single intraperitoneal STZ injection (50 mg/kg; i.p.). MCAO/Re diabetic rats were then treated with NC (50 and 100 mg/kg; bw; p.o.) for two consecutive weeks. The results of the present study showed that oral treatment of MCAO/Re diabetic rats with NC was associated with a marked attenuation of the neurological deficit score as well as the brain imbalance of the redox homeostasis. NC treatment was also associated with decline in the brain expression of tumor necrosis factor, interleukin-1ß, COX-2, cleaved caspase-3, and nuclear factor kappa B. In addition, the expression of glucose transporter 1 proteins upon treatment was restored. PRACTICAL APPLICATIONS: From all these results, it can be concluded that oral supplementation of curcumin nanoemulsion (NC) in diabetic rats reduced the brain injury via augmentation of the expression of glucose transporter 1, as well as its antioxidant and anti-inflammatory properties. Therefore, NC could be delineated as a promising treatment option for cerebral ischemia in diabetic patients.

Virulence of entomopathogenic fungi against Culex pipiens: Impact on biomolecules availability and life table parameters.

Culex pipiens mosquitoes considered as vectors for many arboviruses such as the West Nile virus and encephalitis virus showing a global impact on human health. The natural management of the aquatic stages of this pest is crucial for maintaining an insecticide-free and sustained environment. The present work focused on studying the biological and biochemical effects of the entomopathogenic fungi: Metarhizium anisopliae, Beauveria bassiana, and Paecilomyces lilicanus, against 3rd instar larvae of Culex pipiens laboratory colony. The results revealed that M. anisopliae showed maximum larval mortality (88%) with the lowest lethal time (LT50) (22.6 hrs) at 108 spores/ml followed by B. bassiana (73.33%) with LT50 (38.35 hrs), while P. lilicanus showed minimum percent mortality (65%) with highest LT50 (51.5 hrs). The median lethal concentration (LC50) values were found to be 1.027 × 105 spores/ml for M. anisopliae, 1.24 × 106 spores/ml for B. bassiana, while it was 8.453 × 106 spores/ml for P. lilicanus. A reduction in female fecundity, number of hatched eggs, pupation and adult emergence percentage were recorded. The biochemical analysis of the treated larvae revealed different quantitative decrease in total soluble proteins, lipids, and carbohydrate hydrolyzing enzymes compared to control. Histopathological effects of fungal infection upon insect cuticles, muscles, and midgut were investigated. Based on the obtained results, M. anisopliae proved its superior virulent effect as a bio-control agent against Cx. pipiens.

Degradation of methylene blue using co-dopants Mg and Se in an hydroxyapatite composite.

In this work, a comparative study was made of different magnesium ion content incorporated into hydroxyapatite (HAP) and modified with selenite ions, with the aim to develop the degradation performance of methylene blue. Although the dopant metal (Mg2+ ) was present at a relatively low ratio, it induced a change in the microstructure, morphology, surface area, external surface charge, particle size, and degradation performance. The effect of magnesium and selenium binary doping on microstructure and degradation of methylene blue was evaluated. The external surface charge measured by zeta potential clarified that the highest negativity was -11.8 mV and this was accomplished in 1.0 Mg/Se-HAP. Furthermore, the roughness average increased from 36.8 nm, reaching 59.2 nm upon the addition of Mg(II). Moreover, transmission electron microscope micrographs showed that compositions were formed as rod shapes. The process of degradation was optimized, showing effectiveness in methylene blue degradation of 62.4% after 150 min of exposure to visible light. Electrostatic attraction and H-bonding, and coordination played vital roles in the adsorption process. The recyclability of the as-prepared compositions demonstrated that the effectiveness had been reduced to ~54.2% after five times of re-use.

Effect of a Novel Hybrid Nanocomposite of Cisplatin-Chitosan on Induced Tissue Injury as a Suggested Drug by Reducing Cisplatin Side Effects.

The self-assembly of cisplatin (Cis-Pt) and chitosan nanoparticles (Cs NPs) has been synthesized and characterized successfully by different analyses and techniques, such as scanning electron microscopy, ultraviolet-visible spectrophotometry, and Fourier transform infrared spectroscopy. The efficiency of loading Cis-Pt on Cs NPs for decreasing the side effects of Cis-Pt by loading it on Cs NP surface was revealed through histopathological and physiological measurements for the liver, testis, and kidney cells. Self-assembly hybrid nanocomposite (Cis-Pt@Cs) could improve spermatogenic cells, seminiferous tubules, and Leydig cells in the interstitial tissue. Kidney examination showed intact glomeruli with a mild increase in capsular space in addition to the intact renal tubular epithelial lining, and liver findings showed improvement in dilation and congestion of the central vein besides mild dilation of blood sinusoids in addition to a mild degree of hepatocyte vacuolation. The serum levels of hepatic, renal, and testicular marker analysis were measured, where Cis-Pt increased the serum levels of alanine aminotransferase, aspartate aminotransferase activity, urea, creatinine, and decreased testosterone levels, while synthesized self-assembly appeared normalized levels. From the results, the self-assembly hybrid nanocomposite decreases and improves the side effects of Cis-Pt.

Microstructure, morphology and physicochemical properties of nanocomposites containing hydroxyapatite/vivianite/graphene oxide for biomedical applications.

Designing a nanocomposite that accumulates biocompatibility and antimicrobial behaviour is an essential requirement for biomedical applications. Hydroxyapatite (HAP), graphene oxide, and vivianite in one ternary nanocomposite with three phases and shapes led to an increase in cell viability to 97.6% ± 4 for the osteoblast cells in vitro. The obtained nanocomposites were investigated for their structural features using X-ray diffraction, while the microstructure features were analyzed using a scanning electron microscope (SEM) and a transmission electron microscope. The analysis showed a decrease in the crystal size to 13 nm, while the HAP grains reached 30 nm. The elongated shape of vivianite reached 200 nm on SEM micrographs. The monoclinic and hexagonal crystal systems of HAP and vivianite were presented in the ternary nanocomposite. The maximum roughness peak height reached 236.1 nm for the ternary nanocomposite from 203.3 nm, while the maximum height of the roughness parameter reached 440.7 nm for the di-nanocomposite of HAP/graphene oxide from 419.7 nm. The corrosion current density reached 0.004 µA/cm2 . The ferrous (Fe2+ ) and calcium (Ca2+ ) ions released were measured and confirmed. Therefore, the morphology of the nanocomposites affected bacterial activity. This was estimated as an inhibition zone and reached 14.5 ± 0.9 and 13.4 ± 1.1 mm for Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) after 24 h. The increase in viability and the antibacterial activity refer to the compatibility of the nanocomposite in different medical applications.

Dunalialla salina microalgea and its isolated zeaxanthin mitigate age-related dementia in rats: Modulation of neurotransmission and amyloid-ß protein.

Age-related deterioration of sensorimotor and cognitive abilities suggests that the brain undergoes regressive alterations with aging that compromise its function. Thus, the present study was designed to assess the efficacy of Dunaliella salina in counteracting D-galactose (D-gal)-induced dementia brain aging and its modulatory role in attenuating amyloid ß (Aß) protein and neurotransmitters. Aging associated dementia was generated by injection of D-gal (200 mg/kg; i.p) of rats for 8 weeks. D. salina biomass (250 mg/kg), polar (30 mg/kg), its carotenoid (30 mg/kg) fractions as well as the isolated zeaxanthin (250 µg/kg) were given orally simultaneously with D-gal for additional two weeks. Twenty-four hours after the last treatment dose; behavioral, biochemical and histopathological assessment were performed. Results showed that oral treatment of motor deficit rats with D. salina biomass and its isolated polar and carotenoid fractions showed amelioration in the motor coordination assessed by the rotarod test and in the memory and learning capabilities evaluated by Morris water maze test. D. salina also showed a reduction in brain levels of inflammatory indicators viz. interlekin-1ß and inducible nitric oxide synthetase as well as brain contents of Aß protein and myelin base protein. Likewise, oral treatment with D. salina biomass and its isolated polar and carotenoid fractions exhibited an increase in the rats' brain neurotransmitters and their metabolites. Furthermore, histopathological investigations have confirmed all of these results. Our findings suggest that D. salina overcomes brain aging and thereby repairs age-related dementia, both for its modulating function in attenuating the Aß protein and neurotransmitters.

Antiviral Activity of Zinc Oxide Nanoparticles Mediated by Plumbago indica L. Extract Against Herpes Simplex Virus Type 1 (HSV-1).

INTRODUCTION: Plumbago indica L. is considered a valuable source in the Plumbaginaceae family for various types of active compound such as alkaloids, phenolics and saponins. To promote the usage of P. indica in the bionanotechnology field, zinc oxide nanoparticles (ZnONPs) were biosynthesized by using its alcoholic extract. The inhibitory effects of ZnONPs and the plant extract were also evaluated against HSV-1. METHODS: ZnONPs were described by the following techniques, UV-visible spectroscopy, Fourier transform infrared spectroscopy (FTIR), dynamic light scattering (DLS), zeta potential, scanning electron microscopy (SEM), transmission electron microscopy (TEM) and x-ray diffraction (XRD). The phenolic and flavonoid contents of P. indica extract, which are accountable for bioreduction, formation and stabilization of the nanoparticles, were analyzed by HPLC technique. The antiviral assessment was implemented on both agents by using Vero cell lines. RESULTS: DLS revealed that the average size of ZnONPs was 32.58 ± 7.98 nm and the zeta potential was -20.8 mV. The observation of TEM analysis revealed that the particle size of ZnONPs varied from 2.56 to 8.83 nm. The XRD analysis verified the existence of pure crystals of hexagonal shapes of nanoparticles of ZnO with a main average size of 35.28 nm that is approximating to the values of particle size acquired by SEM analysis (19.64 and 23.21 nm). The HPLC analysis of P. indica ethanolic extract showed that gallic acid, chlorogenic acid and rutin were the major compounds, with concentrations equal to 8203.99, 2965.95 and 1144.99 µg/g, respectively. Regarding the antiviral assessment, the synthesized uncalcinated ZnONPs were found to exhibit a promising activity against HSV-1, with CC50 and IC50 values equal to 43.96 ± 1.39 and 23.17 ± 2.29 µg/mL, respectively. CONCLUSION: The green synthesized ZnONPs are considered promising adjuvants to enhance the efficacy of HSV-1 drugs.