Growth performance,oxidative stress and immune status of newly weaned pigs fed peroxidized lipids with or without supplemental vitamin E or polyphenols

Background:This study evaluated the use of dietary vitamin E and polyphenols on growth,immune and oxidative status of weaned pigs fed peroxidized lipids.A total of 192 piglets(21 days of age and body weight of 6.62±1.04 kg)were assigned within sex and weight blocks to a 2×3 factorial arrangement using 48 pens with 4 pigs per pen.Dietary treatments consisted of lipid peroxidation(6%edible soybean oil or 6%peroxidized soybean oil),and antioxidant supplementation(control diet containing 33 IU/kg DL-α-tocopheryl-acetate;control with 200 IU/kg additional dl-α-tocopheryl-acetate;or control with 400 mg/kg polyphenols).Pigs were fed in 2 phases for 14 and 21 days,respectively.Results:Peroxidation of oil for 12 days at 80°C with exposure to 50 L/min of air substantially increased peroxide values,anisidine value,hexanal,and 2,4-decadienal concentrations.Feeding peroxidized lipids decreased(P<0.001)body weight(23.16 vs.18.74 kg),daily gain(473 vs.346 g/d),daily feed intake(658 vs.535 g/d)and gain:feed ratio(719 vs.647 g/kg).Lipid peroxidation decreased serum vitamin E(P<0.001)and this decrease was larger on day 35(1.82 vs.0.81 mg/kg)than day 14(1.95 vs.1.38 mg/kg).Supplemental vitamin E,but not polyphenols,increased(P≤0.002)serum vitamin E by 84%and 22%for control and peroxidized diets,respectively(interaction,P=0.001).Serum malondialdehyde decreased(P<0.001)with peroxidation on day 14,but not day 35 and protein carbonyl increased(P<0.001)with peroxidation on day 35,but not day 14.Serum 8-hydroxydeoxyguanosine was not affected(P>0.05).Total antioxidant capacity decreased with peroxidation(P<0.001)and increased with vitamin E(P=0.065)and polyphenols(P=0.046)for the control oil diet only.Serum cytokine concentrations increased with feeding peroxidized lipids on day 35,but were not affected by antioxidant supplementation(P>0.05).Conclusion:Feeding peroxidized lipids negatively impacted growth performance and antioxidant capacity of nursery pigs.Supplementation of vitamin E and polyphenols improved total antioxidant capacity,especially in pigs fed control diets,but did not restore growth performance.

Ferroptosis and endoplasmic reticulum stress in ischemic stroke

Ferroptosis is a form of non-apoptotic programmed cell death,and its mechanisms mainly involve the accumulation of lipid peroxides,imbalance in the amino acid antioxidant system,and disordered iron metabolism.The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum,and the progression of inflammatory diseases can trigger endoplasmic reticulum stress.Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival.Ferroptosis and endoplasmic reticulum stress may occur after ischemic stroke.However,there are few reports on the interactions of ferroptosis and endoplasmic reticulum stress with ischemic stroke.This review summarized the recent research on the relationships between ferroptosis and endoplasmic reticulum stress and ischemic stroke,aiming to provide a reference for developing treatments for ischemic stroke.

Ferroptosis mechanism and Alzheimer's disease

Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms.This process plays a crucial role in modulating homeostasis and is evolutionarily conserved across a diverse range of living organisms.Ferroptosis is a classic regulatory mode of cell death.Extensive studies of regulatory cell death in Alzheimer’s disease have yielded increasing evidence that fe rroptosis is closely related to the occurrence,development,and prognosis of Alzheimer’s disease.This review summarizes the molecular mechanisms of ferroptosis and recent research advances in the role of ferro ptosis in Alzheimer’s disease.Our findings are expected to serve as a theoretical and experimental foundation for clinical research and targeted therapy for Alzheimer’s disease.

Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.

Fibroblast growth factor 21 inhibits ferroptosis following spinal cord injury by regulating heme oxygenase-1

Interfering with the ferroptosis pathway is a new strategy for the treatment of spinal cord injury.Fibroblast growth factor 21 can inhibit ferro ptosis and promote neurofunctional recovery,while heme oxygenase-1 is a regulator of iron and reactive oxygen species homeostasis.The relationship between heme oxygenase-1and ferroptosis remains controve rsial.In this study,we used a spinal co rd injury rat model to show that the levels of fibroblast growth factor 21 in spinal co rd tissue decreased after spinal cord injury.In addition,there was a significant aggravation of ferroptosis and a rapid increase in heme oxygenase-1 expression after spinal cord injury.Furthe r,heme oxygenase-1 aggravated fe rroptosis after spinal cord injury,while fibroblast growth factor 21 inhibited fe rroptosis by downregulating heme oxygenase-1.Thus,the activation of fibroblast growth factor 21 may provide a potential treatment for spinal co rd injury.These findings could provide a new potential mechanistic explanation for fibroblast growth factor 21 in the treatment of spinal cord injury.

Metformin alleviates spinal cord injury by inhibiting nerve cell ferroptosis through upregulation of heme oxygenase-1 expression

Previous studies have reported upregulation of heme oxygenase-1 in different central nervous system injury models.Heme oxygenase-1 plays a critical anti-inflammatory role and is essential for regulating cellular redox homeostasis.Metformin is a classic drug used to treat type 2 diabetes that can inhibit ferroptosis.Previous studies have shown that,when used to treat cardiovascular and digestive system diseases,metformin can also upregulate heme oxygenase-1 expression.Therefore,we hypothesized that heme oxygenase-1 plays a significant role in mediating the beneficial effects of metformin on neuronal ferroptosis after spinal cord injury.To test this,we first performed a bioinformatics analysis based on the GEO database and found that heme oxygenase-1 was upregulated in the lesion of rats with spinal cord injury.Next,we confirmed this finding in a rat model of T9 spinal cord compression injury that exhibited spinal cord nerve cell ferroptosis.Continuous intraperitoneal injection of metformin for 14 days was found to both upregulate heme oxygenase-1 expression and reduce neuronal ferroptosis in rats with spinal cord injury.Subsequently,we used a lentivirus vector to knock down heme oxygenase-1 expression in the spinal cord,and found that this significantly reduced the effect of metformin on ferroptosis after spinal cord injury.Taken together,these findings suggest that metformin inhibits neuronal ferroptosis after spinal cord injury,and that this effect is partially dependent on upregulation of heme oxygenase-1.

Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer

BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.

Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer

As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.

Research progress on the anti-colorectal cancer effect of traditional Chinese medicine active ingredients based on ferroptosis

Ferroptosis is defined as an iron-dependent form of regulated cell death that is initiated by the toxic accumulation of lipid peroxides on cellular membranes.In the past decade,ferroptosis has aroused considerable interest in comprehensive treatment of colorectal cancer,mainly as it is a specific cell death mode that is mechanistically and morphologically differ from other forms of cell death such as autophagy,apoptosis,and pyroptosis,following by holding a giant potential for the therapy of colorectal cancer.Research has found that various active ingredients in traditional Chinese medicine possess the ability of inducing ferroptosis in colorectal cancer cells through pathways such as lipid metabolism,iron metabolism,or cysteine/glutamate transporter system,which demonstrating enormous clinical therapeutic potential.In this review,the metabolic regulatory network of ferroptosis is introduced from the perspective of ferroptosis mechanism,and the information on the induction of ferroptosis in colorectal cancer cells by active ingredients of traditional Chinese medicine is also be retrospected,which the purpose is to provide novel strategies for the anti-colorectal cancer therapy of active ingredients in traditional Chinese medicine.

Characteristics of lipids and their feeding value in swine diets

In livestock diets, energy is one of the most expensive nutritional components of feed formulation. Because lipids are a concentrated energy source, inclusion of lipids are known to affect growth rate and feed efficiency, but are also known to affect diet palatability, feed dustiness, and pellet quality. In reviewing the literature, the majority of research studies conducted on the subject of lipids have focused mainly on the effects of feeding presumably high quality lipids on growth performance, digestion, and metabolism in young animals. There is, however, the wide array of composition and quality differences among lipid sources available to the animal industry making it essential to understand differences in lipid composition and quality factors affecting their digestion and metabolism more fully. In addition there is often confusion in lipid nomenclature, measuring lipid content and composition, and evaluating quality factors necessary to understand the true feeding value to animals. Lastly, advances in understanding lipid digestion, post-absorption metabolism, and physiological processes（e.g., cell division and differentiation, immune function and inflammation）; and in metabolic oxidative stress in the animal and lipid peroxidation, necessitates a more compressive assessment of factors affecting the value of lipid supplementation to livestock diets. The following review provides insight into lipid classification, digestion and absorption, lipid peroxidation indices, lipid quality and nutritional value, and antioxidants in growing pigs.

Erythropoietin inhibits ferroptosis and ameliorates neurological function after spinal cord injury

Ferroptosis is one of the critical pathological events in spinal cord injury.Erythropoietin has been reported to improve the recovery of spinal cord injury.However,whether ferroptosis is involved in the neuroprotective effects of erythropoietin on spinal cord injury has not been examined.In this study,we established rat models of spinal cord injury by modified Allen’s method and intraperitoneally administered 1000 and 5000 IU/kg erythropoietin once a week for 2 successive weeks.Both low and high doses of erythropoietin promoted recovery of hindlimb function,and the high dose of erythropoietin led to better outcome.High dose of erythropoietin exhibited a stronger suppressive effect on ferroptosis relative to the low dose of erythropoietin.The effects of erythropoietin on inhibiting ferroptosis-related protein expression and restoring mitochondrial morphology were similar to those of Fer-1(a ferroptosis suppressor),and the effects of erythropoietin were largely diminished by RSL3(ferroptosis activator).In vitro experiments showed that erythropoietin inhibited RSL3-induced ferroptosis in PC12 cells and increased the expression of xCT and Gpx4.This suggests that xCT and Gpx4 are involved in the neuroprotective effects of erythropoietin on spinal cord injury.Our findings reveal the underlying anti-ferroptosis role of erythropoietin and provide a potential therapeutic strategy for treating spinal cord injury.

Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice

Recent studies have shown that chlorogenic acid(CGA),which is present in coffee,has protective effects on the nervous system.However,its role in neonatal hypoxic-ischemic brain injury remains unclear.In this study,we established a newborn mouse model of hypoxic-ischemic brain injury using a modified Rice-Vannucci method and performed intraperitoneal injection of CGA.We found that CGA intervention effectively reduced the volume of cerebral infarct,alleviated cerebral edema,restored brain tissue structure after injury,and promoted axon growth in injured brain tissue.Moreover,CGA pretreatment alleviated oxygen-glucose deprivation damage of primary neurons and promoted neuron survival.In addition,changes in ferroptosis-related proteins caused by hypoxic-ischemic brain injury were partially reversed by CGA.Furthermore,CGA intervention upregulated the expression of the key ferroptosis factor glutathione peroxidase 4 and its upstream glutamate/cystine antiporter related factors SLC7A11 and SLC3A2.In summary,our findings reveal that CGA alleviates hypoxic-ischemic brain injury in neonatal mice by reducing ferroptosis,providing new ideas for the treatment of neonatal hypoxic-ischemic brain injury.

Vicious cycle of lipid peroxidation and iron accumulation in neurodegeneration

Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.Mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.

Mesenchymal stem cells,extracellular vesicles,and transcranial magnetic stimulation for ferroptosis after spinal cord injury

Spinal cord injury is characte rized by diffe rent aetiologies,complex pathogenesis,and diverse pathological changes.Current treatments are not ideal,and prognosis is generally poor.After spinal cord injury,neurons die due to various forms of cell death.Among them,fe rroptosis causes dysfunction after spinal cord injury,and no existing traditional treatments have been indicated to block its occurrence.Meanwhile,emerging therapies using mesenchymal stem cells,extracellular vesicles,and transcranial magnetic stimulation therapy are promising for reve rsing spinal co rd neuronal ferroptosis after spinal cord injury.However,no definitive studies have demonstrated the effectiveness of these approaches.This review summarizes the existing research on the mechanisms of ferroptosis;fe rroptosis after spinal cord injury;treatment of spinal cord injury with mesenchymal stem cells,extracellular vesicles,and transc ranial magnetic stimulation;and treatment of ferroptosis using mesenchymal stem cells,extracellular vesicles,and transc ranial magnetic stimulation.Inhibiting ferroptosis can promote the reversal of neurological dysfunction after spinal cord injury.In addition,mesenchymal stem cells,extracellular vesicles,and transc ranial magnetic stimulation can reve rse adverse outcomes of spinal cord injury and regulate ferroptosis-related fa ctors.Thus,it can be inferred that mesenchymal stem cells,extracellular vesicles,and transcranial magnetic stimulation have the potential to inhibit fe rroptosis after spinal cord injury.This review serves as a reference for future research to confirm these conclusions.

Cardioprotective effects of Pinus eldarica bark extract on adrenaline-induced myocardial infarction in rats

Objective:To investigate the effect of Pinus eldarica bark extract on adrenaline-induced myocardial infarction.Methods:Hydroalcoholic extract was prepared using maceration method and its total phenolic content was determined using the Folin-ciocalteu method.Pretreatment was done by oral administration of 100,200,and 400 mg/kg Pinus eldarica bark extract for 16 days in male Wistar rats.Injection of adrenaline(2 mg/kg,s.c.)was performed on the 15th and 16th days for induction of myocardial infarction.LeadⅡEEG was recorded.Serum cardiac marker enzymes and antioxidative parameters were evaluated and a histopathological examination of heart tissues was performed.Results:Pretreatment with Pinus eldarica bark extract especially at its high doses significantly lowered the ST-segment elevation,improved heart rate,and decreased RR interval in ECG pattern of rats with adrenaline-induced myocardial infarction.It declined serum markers of heart damage including aspartate aminotransferase,lactate dehydrogenase,and creatine phosphokinase-MB,and also decreased lipid peroxidation marker,and heart weight while raising total antioxidant capacity and considerably improved histopathological alterations of the heart induced by adrenaline.Conclusions:Pinus eldarica bark extract shows beneficial cardioprotective and antioxidant effects against adrenaline-induced myocardial infarction.It can be further explored as a potential treatment for myocardial infarction.

Effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7S)and glycinin(11S)

This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidation method.Functional properties were analyzed based on emulsifying and foaming properties.The potential allergenicity was evaluated by in vitro and in vivo methods.The results found that oxidation altered structures of the proteins and resulted in the formation of cross-linked protein polymers.The emulsion and foaming properties of the proteins were improved after oxidation.The IgE-binding capacity of 7 S and11 S reduced after oxidation.KU812 cell assays showed that both histamine and IL-4 release decreased after oxidation treatment.A mouse model showed that oxidation reduced the IgE,IgG,and IgG1 levels,as well as reduced histamine and mMCP-1 release in serum,which might suppress the allergic reaction.In conclusion,the lipid peroxidation treatment likely causes changes to the functional properties of soybean,decreasing the potential allergenicity of 7 S and 11 S.

Fe-dependent cellular alterations of oxidative balance in aquatic organisms.Could be ferroptosis involved?

The purpose of this review is to briefly summarize the central role of iron(Fe)in terms of cellular alterations of the oxidative/protective balance with special emphasis on its possible involvement in ferroptosis-dependent disruption in aquatic organisms.In ferroptotic cells or tissues,the intracellular Fe level increases;meanwhile the treatment with Fe chelators limits ferroptosis.Eukaryotic algae can assimilate Fe from the environment through several mechanisms,and aquatic animals incorporate dissolved Fe and Fe bound to both inorganic particles and organic matter.The central role of lipid peroxidation mediating ferroptosis was demonstrated in some algae where both low and high Fe concentrations could induce oxidative stress and programmed cell death.Aquatic animals have high levels of polyunsaturated fatty acids and numerous studies have analyzed Fe effects on the lipidic fraction which could be related to ferroptosis.The ferroptosis reaction can be regulated through the antioxidant defense system,in combination with the protein degradation structure,metabolism,and gene transcription.Early depletion of nonenzymatic antioxidants like reduced glutathione(GSH)in animals,and the reduction of both GSH and ascorbate in photosynthetic organisms,are characteristic features of ferroptosis.Therefore,ferroptosis can be prevented if Fe chelators,certain antioxidants,and specifically regulating genes are activated.Thus,the global scenario for the Fe role as a toxic component in biological systems seems to be even more complicated than it was previously understood.Much more research on this subject is needed to improve the life span and survival of aquatic organisms after exposure to natural and anthropogenic adverse conditions.

Interaction mechanisms between autophagy and ferroptosis:Potential role in colorectal cancer

Colorectal cancer(CRC)is a common malignancy that has the second highest incidence and mortality rate.Although there are many personalized treatment options for CRC,the therapeutic effects are ultimately limited by drug resistance.Studies have aimed to block the initiation and progression of CRC by inducing cell death to overcome this obstacle.Substantial evidence has indicated that both autophagy and ferroptosis play important regulatory roles in CRC.Autophagy,a lysosome-dependent process by which cellular proteins and organelles are degraded,is the basic mechanism for maintaining cell homeostasis.The duality and complexity of autophagy in cancer therapy is a hot topic of discussion.Ferroptosis,a regulated cell death pathway,is associated with iron accumulationinduced lipid peroxidation.The activation of ferroptosis can suppress CRC proliferation,invasion and drug resistance.Furthermore,recent studies have suggested an interaction between autophagy and ferroptosis.Autophagy can selectively degrade certain cellular contents to provide raw materials for ferroptosis,ultimately achieving antitumor and anti-drug resistance.Therefore,exploring the interaction between autophagy and ferroptosis could reveal novel ideas for the treatment of CRC.In this review,we describe the mechanisms of autophagy and ferroptosis,focusing on their roles in CRC and the crosstalk between them.

Targeting biosignatures of hyperglycemia and oxidative stress in diabetes comorbid depressive rats: effectiveness of hydroethanolic extract of the whole plant of Ludwigia octovalvis

Background:The prime objective of the current research was to evaluate the whole plant hydroalcoholic extract of Ludwigia octovalvis(HLO)against hyperglycemia,and oxidative stress biomarkers in rats induced with diabetes comorbid depression,diabetes comorbid depression(streptozotocin-nicotinamide+electric footshocks).Methods:2,2-Diphenyl-1-picrylhydrazyl assay of HLO versus ascorbic acid was done.Effects of 200 and 400 mg/kg body weight/day HLO doses versus 25 mg/kg body weight/day metformin was studied through insulin,glucose,superoxide dismutase,lipid peroxidation,catalase,and behavioral assessment(forced swim and open field tests).Results:IC50 values of HLO and ascorbic acid were 33.52 and 27.86μg/mL respectively.Both the HLO doses showed intended results with respect to oxidative stress biomarkers in diabetes comorbid depression rats in comparison to metformin.Open field test showed better results for HLO in diabetes comorbid depression rats.However,hypoglycemic effects,and forced swim test performance of metformin was slightly higher than the 400 mg dose,followed by the 200 mg dose of HLO.Ethyl gallate,gallic acid,β-sitosterol,and quercetin in HLO might resulted in attenuating diabetic as well as depression biomarkers.Conclusion:Inhibition of glucosidase and lipase activity,and AMP-activated protein kinase phosphorylation might be the possible biochemical changes occurred in HLO treated rats.

Anticancer Activity of Peganum harmala and Haloxylon salicornicum Leaf Extracts on Lung Cancer A549 and Prostate Cancer PC-3 Cell Lines

Cancer is a worldwide disease that ranks as the second-largest cause of death after cardiovascular disease. In 2019, the estimated number of cancer deaths was around 10 million worldwide and 600,000 in the United States. Due to the high side effects of the available treatments for cancer, such as chemotherapy and radiotherapy, a demand for alternative treatments has been a goal for scientists with less toxicity and side effects. Lung cancer is the most common type of cancer worldwide and the leading cause of death in the United States. In addition, prostate cancer is the second-leading cause of cancer death in American men after lung cancer. Natural sources discovered to have therapeutic medicinal properties against human diseases are the plants Peganum harmala and Haloxylon salicornicum. The aim of this study is to test the anticancer activity of leaf extracts of Peganum harmala and Haloxylon salicornicum on lung cancer (A549) and prostate cancer (PC3) cell lines. The anticancer activity of P. harmala and H. salicornicum was studied using the assays: crystal violet viability, lipid peroxidation, and caspase-3 techniques, which were evaluated in vitro on two human cancer cell lines. The results of the study showed that both plants’ extracts reduced the viability of both cancer cell lines, which depended on the concentration of the extract. Also, P. harmala showed more potent activity against both types of cancer than H. salicornicum. P. harmala and H. salicornicum decreased the lipid peroxidation that induces cancer as well as increased the expression of caspase-3, which causes apoptosis and cell death. This study concluded that P. harmala and H. salicornicum leaf extracts showed significant anticancer properties, which might be due to the presence of phytochemicals, including flavonoids and phenolics.