Palm oil amends serum female hormones, ovarian antioxidants, inflammatory markers, and DNA fragmentation in favism-induced female rats.

BACKGROUND: Favism is a metabolic disease and this study evaluates the effectiveness of palm oil and its triacylglycerol constituent in favism-induced female rats to restore serum female hormones, ovarian antioxidants, inflammatory markers, and DNA fragmentation. METHODS: Animals were 36 female albino rats. They classified to two equal (normal and favism) groups. The normal group was divided into three equal subgroups: the control, palm oil, and triacylglycerol subgroups. The normal rats were given 1 mL of saline, 1 mL of palm oil, and 1 mL of triacylglycerol orally, respectively. The Favism group was classified also into three equal subgroups: the favism group, the favism + palm oil, the Favism + triacylglycerol. The favism rats were given 1 mL of saline, 1 mL of palm oil, and 1 mL of triacylglycerol orally. For four weeks, all treatments were administered orally via oral gavage once daily. RESULTS: The hemoglobin, hematocrite, the blood cells, glucose and glucose-6-phosphate dehydrogenase, and liver function were decreased in favism. Female hormones such as serum luteinizing hormone, follicle stimulating hormone, Estrone, Estriol, 17α-Estradiol, 17ß-Estradiol, and Estradiol-17-ß-stearate were decreased in favism. Ovarian antioxidants were decreased while ovarian inflammatory markers were increased in favism. Favism induced ovarian DNA apoptosis. Furthermore, oral administration with palm oil or its triacylglycerol constituent in favism-induced female rats restored all these parameters to be approached the control levels. CONCLUSIONS: Palm oil restored serum female hormones, ovarian antioxidants, inflammatory markers, and DNA fragmentation in favism-induced female rats and this effect related to oil triacylglycerol constituent.

Luteolin amends neural neurotransmitters, antioxidants, and inflammatory markers in the cerebral cortex of Adderall exposed rats.

BACKGROUND: Adderall is a central nervous system stimulant while luteolin has neuroprotective activity. This study aimed to determine whether luteolin can amend neural neurotransmitters, antioxidants, and inflammatory markers in the cerebral cortex of Adderall exposed rats. METHODS: Thirty-six male albino rats were divided into 6 equal groups, Control, Luteolin (1 g/kg)-treated, and Luteolin (2 g/kg)-treated groups: normal rats were orally administrated once a day with 2 ml distilled water, luteolin (1 g/kg), and luteolin (2 g/kg), respectively for 4 weeks. Adderall rats, Adderall rats + luteolin (1 g/kg)-treated, and Adderall rats + luteolin (2 g/kg)-treated groups: normal rats were orally administrated once a day with 10 mg/kg of Adderall, 3 days/week for 4 weeks, then these rats orally administrated daily once a day with 2 ml of distilled water, luteolin (1 g/kg), and luteolin (2 g/kg), respectively for another 4 weeks. RESULTS AND CONCLUSION: Adderall decreased superoxide dismutase, glutathione peroxidase, catalase, NADPH oxidase, interleukin-10, serotonin, dopamine, norepinephrine, γ-aminobutyric acid, and acetylcoline estrase but increased malondialdehyde, conjugated dienes, oxidative index, tumour necrosis factor-α, interleukin-1ß, and interleukin-6 levels in the cerebral cortex. Adderall increased the expression of glial fibrillary acidic protein, ionized calcium binding adaptor molecule 1, and anti-calbindin in the cerebral cortex of Adderall-treated rats. In Adderall-treated rats, daily oral administration of luteolin for 4 weeks brought all these parameters back to values that were close to control where higher dose was more effective than lower dose. The importance of this research is to provide natural compound that amends Adderall-related neural disturbances and this natural compound is cheap, avaliable without any side effect and it does not interfer with Adderall efficiency.

Shikimic acid recovers diarrhea and its complications in SD rats fed lactose diet to induce diarrhea.

BACKGROUND: Diarrhea is the increase of excretion of human water content and an imbalance in the physiologic processes of the small and large intestine while shikimic acid is an important biochemical metabolite in plants. This study aims to study the anti-diarrheal activity of shikimic acid through restoring kidney function, antioxidant activity, inflammatory markers, sodium/potassium-ATPase activity, apoptosis genes, and histology of the kidney in SD rats fed lactose diet to induce diarrhea. RESULTS: Thirty-six male SD rats (150 ± 10 g, 12 weeks old) were divided into 2 equal groups (18 rats/group) as follows: normal and diarrheal rats. Normal rats were divided into 3 equal groups of 6 rats each: the control, shikimic acid, and desmopressin drug groups. Diarrheal rats were also divided into 3 equal groups of 6 rats each: diarrheal, diarrheal rats + shikimic acid, and diarrheal rats + desmopressin drug groups. Shikimic acid restored serum urea and creatinine, urinary volume, kidney weight, sodium, potassium, and chloride balance in serum and urine. The acid returned the antioxidant (superoxide dismutase, glutathione peroxidase, catalase, malondialdehyde, NADPH oxidase activity, conjugated dienes, and oxidative index) activity and the inflammatory markers (tumor necrosis factor-α, interleukin-1ß, interleukin-6, and interleukin-10) to values approaching the control values. Shikimic acid also restored the sodium/potassium-ATPase activity, the apoptosis genes p53 and bcl-2, and the histology of kidney tissue in diarrheal rats to be near the control group. CONCLUSIONS: Shikimic acid rescues diarrhea and its complications through restoring kidney function, serum and urinary electrolytes, antioxidant activity, inflammatory markers, sodium/potassium-ATPase activity, the apoptosis genes, and the histology of the kidney in diarrheal rats to approach the control one.

Linalool attenuates hypothalamus proteome disturbance facilitated by methamphetamine induced neurotoxicity in rats.

BACKGROUND: One of the most powerful stimulants of the central nervous system is methamphetamine (METH). Linalool has a neuroprotective effect against ischemia injury by reducing oxidative stress and apoptosis. The present study investigated whether linalool can reverse the hypothalamus neurotoxicity and proteome disturbance in METH-treated rats. BRIEF METHOD: A total of 36 male albino rats were split into two equal groups (normal and METH-treated). Three equal subgroups of normal rats were created; Control, Linalool (25 mg/kg), and Linalool (50 mg/kg); Normal rats were given daily oral doses of 1 ml of distilled water, 25 mg/kg linalool, and 50 mg/kg of linalool, respectively. METH groups were divided into 3 equal subgroups; METH-treated rats, Linalool (25 mg/kg)+METH-treated, and Linalool (50 mg/kg)+METH-treated subgroups; METH-treated rats received daily and oral doses of 1 ml distilled water, 25 mg/kg linalool, and 50 mg/kg of linalool, respectively. RESULTS: According to the data obtained, METH caused a decrease of the sucrose preference test, travel distance test, and center square entries test, superoxide dismutase, glutathione peroxidase, catalase, NADPH oxidase, interleukin-10 but a rise in the center square duration test, tail suspension test, and forced swimming test, malondialdehyde, conjugated dienes, oxidative index, serotonin, dopamine, norepinephrine, γ-aminobutyric acid, tumour necrosis factor-α, interleukin-1ß, interleukin-6 levels. When compared to the control group, rats treated with METH had lower sodium/potassium ATPase activity and missing of prothrombin, fibrinogen, and ceruloplasmin protein bands in the hypothalamus. In METH-treated rats, daily and oral co-administration with linalool brought all these parameters back to values that were close to control. SIGNIFICANCE: According to obtained data, linalool could protect the hypothalamus against METH-induced neurotoxicity and proteome disturbance probably by modifying oxidative stress, neurotransmitters, inflammation, sodium/potassium-ATPase activity, proteome disturbance, and tissue histology in METH-treated rats where higher dose of linalool was more efficient than lower dose.

Malic Acid Improves Behavioral, Biochemical, and Molecular Disturbances in the Hypothalamus of Stressed Rats.

BACKGROUND: Stress can lead to emotional and mental symptoms such as anxiety, sadness, panic attacks, and depression. Malic acid was chosen due to malic acid has the ability to improve antioxidant activity and improves liver damage. This study evaluates malic acid anti-depressant activity in the hypothalamus of stressed rats. METHODS: Thirty-six male albino rats were divided into 2 equal groups; Normal and chronic mild stress (CMS) rats. Normal rats were divided into 3 equal groups; control, malic acid, and venlafaxine drug groups: normal rats were administered orally with 1 mL of saline solution, 250 mg/kg of malic acid, and 20 mg/kg of venlafaxine drug, respectively. CMS rats were divided into 3 equal groups; CMS, CMS + malic acid, and CMS + venlafaxine drug: CMS rats were administered orally with 1 mL of saline solution, 250 mg/kg of malic acid, and 20 mg/kg of venlafaxine drug, respectively. All the above-mentioned treatments were administered once a day by oral gavage for 6 weeks. RESULTS: The obtained results revealed that the animal behavioral tests such as forced swimming test, tail suspension test, sucrose preference test, and open-field test (center square entries test, center square duration test, and distance travelled test), norepinephrine, dopamine, serotonin, γ-aminobutyric acid, nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity, oxidative index, conjugated dienes, catalase, glutathione peroxidase, superoxide dismutase, malondialdehyde, interleukin-6, tumor necrosis factor-α, interleukin-10, interleukin-1ß, sodium/potassium-ATPase activity, and histamine-N-methyl transferase (Hnmt) and tyrosine hydroxylase (TH) enzymes in the hypothalamus of stressed rats, were returned to approaching the normal state in the stressed group after treating with malic acid for 6 weeks. CONCLUSIONS: Malic acid ameliorated stressed-related symptoms and it inhibited superoxide anion and neuro-inflammation in the hypothalamus of stressed rats.

Fisetin Treats Kidney Oxidative Stress, Inflammation, and Apoptosis in Rat Diarrhea.

BACKGROUND: Diarrhea is the increase in the excretion of human water; meanwhile, fisetin, a bioactive flavonol molecule, is widely used in the treatment/prevention of gastrointestinal disorders. The purpose of this study is to investigate the anti-diarrheal activity of fisetin by restoring kidney function, antioxidant activity, inflammatory markers, Na+/K+-ATPase level, apoptosis, and protein content in diarrheal rats. METHODS: A total of 36 male rats were distributed into two groups (18 rats/group): normal and diarrheal. The normal group was further divided into three subgroups (6 rats/subgroup): Control, fisetin, and desmopressin drug subgroups, consisting of normal rats orally treated once a day for 4 weeks with 1 mL distilled water, 50 mg/kg fisetin, and 1 mg/kg desmopressin drug, respectively. A lactose diet containing 35% lactose was fed to the normal rats for a month. The diarrheal rats were also divided into three subgroups (6 rats/subgroup): diarrheal rats, diarrheal rats + fisetin, and diarrheal rats + desmopressin drug groups, whereby the diarrheal rats were orally treated once a day for 4 weeks with 1 mL distilled water, 50 mg/kg fisetin, and 1 mg/kg desmopressin drug, respectively. RESULTS: Fisetin significantly decreased serum urea (41.20 ± 2.6-29.74 ± 2.65), creatinine (1.43 ± 0.05-0.79 ± 0.06), and urinary volume (1.30 ± 0.41-0.98 ± 0.20), while significantly increasing kidney weight (0.48 ± 0.03-0.67 ± 0.07), sodium, potassium, and chloride balance in both serum and urine. Fisetin significantly increased the antioxidant activity (superoxide dismutase (1170 ± 40-3230 ± 50), glutathione peroxidase (365 ± 18-775 ± 16), catalase (0.09 ± 0.03-0.14 ± 0.06), and nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase activity (8.6 ± 1.31-10.5 ± 1.25), while significantly decreasing malondialdehyde (19.38 ± 0.54-9.54 ± 0.83), conjugated dienes (1.86 ± 0.24-1.64 ± 0.19), and oxidative index (0.62 ± 0.04-0.54 ± 0.05)), alongside the inflammatory markers (tumor necrosis factor-α (65.2 ± 2.59-45.3 ± 2.64), interleukin-1ß, interleukin-6 (107 ± 4.5-56.1 ± 7.2), and interleukin-10) in the diarrheal rats to values approaching the control values. Fisetin also restored the Na+/K+-ATPase level, apoptosis, protein content, and kidney architecture in diarrheal rats to be near the control group. CONCLUSIONS: Fisetin treated diarrhea in rats by restoring kidney function, antioxidant activity, inflammatory markers, apoptosis, proteome content, and histology.

Sinapic acid restores blood parameters, serum antioxidants, and liver and kidney functions in obesity.

Obesity is an additional body fat that causes a harmful effect on human health while sinapic acid (SA) is a phyto-constituent presents in spices, citrus, berry fruits, and vegetables. This study evaluates SA to amend blood parameters, serum glucose, proteins, lipids, and antioxidants, and liver and kidney functions in obese rats. Thirty male albino rats were divided into 2 groups (normal and obese rats). The normal, non-obese rats subdivided into 2 subgroups; Control and SA (40 mg/kg) subgroup: daily oral intake of 1 ml saline and 40 mg/kg SA, respectively once a day. The obese rats subdivided also into 3 subgroups; Obese, Obese + SA (20 mg/kg), and Obese + SA (40 mg/kg)-treated groups which received no treatment, 20 mg/kg SA, and 40 mg/kg SA, respectively once a day. All treatments were orally administrated for 1 month. The results showed that obesity caused an increase in body and organ weight, serum total cholesterol, triglycerides, low density lipoproteins, malondialdehyde, nitric oxide, glucose, bilirubin and blood urea nitrogen while decrease serum superoxide dismutase, glutathione peroxidase, glutathione, glutathione reductase, glutathione-S-transferase, hemoglobin, hematocrite, red blood cells, white blood cells, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, urea, creatinine, and uric acid compared to control group. Obesity caused disappearance of prothrombin and fibrinogen proteins and damages to liver and kidney tissues. The oral administration with SA daily for 1 month in obese rats returned all these parameters to the control values where the higher dose of SA was more effective than the lower dose. In conclusion, SA restores body and organ weight, blood parameters, serum glucose, proteins, lipids, antioxidants, and liver and kidney functions in obesity.

Micro-needling versus fractional carbon dioxide laser for delivery of tranexamic acid in the treatment of melasma: A split-face study.

BACKGROUND: Tranexamic acid (TXA) in oral, topical, and intra-dermal injection routes showed efficacy in melasma treatment. Micro-needling and fractional carbon dioxide (CO2 ) laser were reported to enhance the drug delivery of TXA. AIMS: This study aimed at comparing the use of micro-needling and fractional CO2 laser for drug delivery of TXA in the treatment of facial melasma. PATIENTS/METHODS: Thirty female patients with bilateral symmetrical facial melasma were subjected to micro-needling, for one side of the face, and fractional CO2 laser, for the other, followed by an immediate topical application of TXA solution 4 mg/mL. Patients received six biweekly sessions. RESULTS: Two weeks after the last session, a significant reduction in baseline modified melasma area and severity index (mMASI) score was observed on both sides. The mean ± SD baseline mMASI dropped from 3.43 ± 1.84 to 1.59 ± 1.51 (mean reduction 57.73%, P < .001) and from 3.51 ± 1.84 to 1.78 ± 1.51 (mean reduction 55.82%, P < .001) in the micro-needling-treated side and in the fractional CO2 laser-treated side, respectively. However, no statistically significant differences were found between the two sides (P = .81). CONCLUSIONS: Micro-needling and fractional CO2 laser are equally safe and effective for the delivery of TXA in the treatment of facial melasma.

HSF3 and Hsp70 Expression during Post-Hatch Cold Stress in Broiler Chickens Subjected to Embryonic Thermal Manipulation.

Decades of selective breeding for commercial purposes have rendered the broiler chicken (Gallus gallus domesticus) highly susceptible to heat and cold stress. A multitude of studies have documented the effects of thermal manipulation (TM) on broiler thermotolerance during periods of post-hatch heat stress, but very few have focused on the effect of TM on a broiler's ability to withstand cold stress. Therefore, the primary objective of the current study is to determine the effects of TM on the acquisition of thermotolerance in broilers via their expression of the stress-associated 70 kilodalton heat shock protein (Hsp70) gene and heat shock factor 3 (HSF3) gene. Briefly, Hubbard broiler embryos were subject to TM by increasing the incubation temperature to 39 °C and 65% relative humidity (RH) for 18 h daily, from embryonic days (ED) 10 to 18. Broilers were then exposed to cold stress by decreasing the room temperature to 16 °C during post-hatch days 32 to 37. After thermal challenge, broilers were euthanized and hepatic and splenic tissues were collected. Our results showed that TM decreased the hatchability rate and body temperature but improved the body weight gain. TM generally decreased the hepatic expression but did not change the splenic expression of HSF3 during cold stress. In contrast, both hepatic and splenic Hsp70 expression decreased during cold stress. The results of the present study may suggest that TM significantly affects a broiler's genetic response to cold stress.

Embryonic Thermal Manipulation Affects the Antioxidant Response to Post-Hatch Thermal Exposure in Broiler Chickens.

Thermal stress is a major source of oxidative damage in the broiler chicken (Gallus gallus domesticus) due to the latter's impaired metabolic function. While heat stress has been extensively studied in broilers, the effects of cold stress on broiler physiologic and oxidative function are still relatively unknown. The present study aimed to understand how thermal manipulation (TM) might affect a broiler's oxidative response to post-hatch thermal stress in terms of the mRNA expression of the catalase, NADPH oxidase 4 (NOX4), and superoxide dismutase 2 (SOD2) genes. During embryonic days 10 to 18, TM was carried out by raising the temperature to 39 °C at 65% relative humidity for 18 h/day. To induce heat stress, room temperature was raised from 21 to 35 °C during post-hatch days (PD) 28 to 35, while cold stress was induced during PD 32 to 37 by lowering the room temperature from 21 to 16 °C. At the end of the thermal stress periods, a number of chickens were euthanized to extract hepatic and splenic tissue from the heat-stressed group and cardiac, hepatic, muscular, and splenic tissue from the cold-stressed group. Catalase, NOX4, and SOD2 expression in the heart, liver, and spleen were decreased in TM chickens compared to controls after both cold and heat stress. In contrast, the expression levels of these genes in the breast muscles of the TM group were increased or not affected. Moreover, TM chicks possessed an increased body weight (BW) and decreased cloacal temperature (TC) compared to controls on PD 37. In addition, TM led to increased BW and lower TC after both cold and heat stress. Conclusively, our findings suggest that TM has a significant effect on the oxidative function of thermally stressed broilers.

Oral supplementation with geranium oil or anise oil ameliorates depressed rat-related symptoms through oils antioxidant effects.

Background Depression is a psychiatric disease condition and the chronic mild stress (CMS) model is a well-known and valuable animal model of depression. Geranium oil and anise oil were chosen for such a study. The aim of this research was to establish the geranium oil and anise oil effect to ameliorate CMS-related symptoms. Methods This research included 80 male albino rats each group of 10 rats and the animals were divided into two major groups: normal and CMS. The normal group was subdivided into four (control, geranium oil, anise oil and venlafaxine drug) subgroups treated orally with saline, geranium oil, anise oil and venlafaxine drug, respectively, for 4 weeks. The CMS group was subdivided into four (CMS without any treatment, CMS + geranium oil, CMS + anise oil and CMS + venlafaxine drug) subgroups treated orally with geranium oil, anise oil and venlafaxine drug, respectively, for 4 weeks. Results The sucrose consumption in sucrose preference test, the distance traveled test and center square entries test were decreased, while center square duration test, immobility time in tail suspension test and floating time in forced swimming test were increased in CMS. The superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase levels decreased but malondialdehyde and nitric oxide levels increased in brain cerebral cortex and hippocampus areas in CMS. The oral intake of geranium oil and anise oil pushes all these parameters to approach the control levels. These results were supported by histopathological investigations of both brain cerebral cortex and hippocampus tissues. Conclusions Geranium oil and anise oil ameliorate CMS-related symptoms and this effect were related to the antioxidant effects of oils.

Effect of Acute Heat Stress on the mRNA Levels of Cytokines in Broiler Chickens Subjected to Embryonic Thermal Manipulation.

Heat stress significantly impacts the immunity and cytokine expression of chickens. However, the effects of embryonic thermal manipulation (TM) on cytokine expression in broiler chickens (broilers) is unclear. The objective of the current study was to evaluate the effects of TM on the splenic mRNA expression dynamics of certain cytokines-namely, IFN-α, IFN-ß, IFN-γ, IL-4, IL-8, IL-15, IL-16, IL-17, and IL-18-in broilers during subsequent exposure to acute heat stress (AHS). TM was performed by elevating the incubation temperature to 39 °C at 65% relative humidity (RH) for 18 h daily during embryonic days (ED) 10-18. On post-hatch day 28, AHS was carried out for 7 h at 40 °C. At 0 h and after 1, 3, 5, and 7 h of AHS, splenic tissues were collected from all study groups to evaluate mRNA expression by relative-quantitative real-time (RT)-PCR. Plasma was collected to measure IL-4, IL-8, and IFN-γ levels. At 0 h, TM significantly reduced the basal mRNA level of IFN-ß and the plasma level of IFN-γ and IL-8. Moreover, AHS significantly decreased IFN-ß in control chicks, decreased IL-4 in both TM and control chicks, and increased IFN-γ and IL-16 in TM chicks. IFN-α, IL-8, IL-15, IL-17, and IL-18 expression all significantly increased during AHS in both TM and control chicks, but expression dynamics were improved in TM chicks for all cytokines (except IL-17). AHS resulted in increased plasma IFN-γ levels in TM chicks only, and increased IL-8 levels at 3 and 5 h of AHS in TM chicks, but at 7 h in control chicks. Lastly, 3 h of AHS increased IL-4 plasma levels in control chicks. The results of this study may indicate that TM has a long-term effect on cytokine expression dynamics of broilers, especially during AHS. Therefore, TM may improve heat tolerance acquisition by increasing the expression of signaling proteins important to tissue stability and to repair mechanisms that are employed during and/or after heat stress recovery.

Fertaric Acid Protects from Octylphenol-Related Hepatotoxicity in Rats: Biochemical, Molecular, and Histopathological Studies.

The endocrine-disrupting chemical 4-tert-octylphenol (OP) can mimic estrogen and testosterone hormones and threaten health; fertaric acid (FA) is a hydroxycinnamic acid found in grapefruit. This study aimed to investigate whether FA has a protective effect on 4-tert-octylphenol-related hepatotoxicity. Thirty male albino rats were divided into 5 equal groups of 6 rats each as follows: control group-administrated orally with 1 ml saline 3 days/week for 4 weeks; corn oil group-administrated orally with 1 ml corn oil 3 days/week for 4 weeks; FA-treated group-administrated orally with FA (45 mg /kg body weight) dissolved in saline 3 days/week for 4 weeks; OP-treated group-administrated orally with OP (40 mg /kg body weight) dissolved in corn oil 3 days/week for 4 weeks; FA + OP-treated group-administrated orally with FA (45 mg /kg body weight) dissolved in saline 3 days/week for 4 weeks then administrated orally with OP (40 mg/kg body weight) dissolved in corn oil 3 days/week for another 4 weeks. The results obtained showed that OP-exposed rats had significant increase in serum aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transferase, lactate dehydrogenase, bilirubin, serum and liver tumor necrosis factor-α, interleukin-1ß and malondialdehyde, serum interleukin-6 and interleukin-10 and significant decrease in serum alkaline phosphatase, acid phosphatase, serum and liver superoxide dismutase, glutathione peroxidase, and catalase. OP caused an inhibitory action on the gene expression of liver proteins. Rats treated with FA before OP exposure had near-normal values. In addition, FA prevented the degradation of liver deoxyribonucleic acid (DNA), and DNA reformation occurred. In conclusion, FA protects from dangerous OP-related hepatic effects, and these results were supported by molecular and histological investigations.

Acute and subacute toxicity of Ammi visnaga on rats.

Ammi visnaga (Av) is a source of khellin where a tea made from the fruit of this plant was used as herbal medicine for kidney stones in Egypt. In the present research, the acute and subacute toxicity studies with oral intake of 150, 300 and 600 mg/kg of Av seed ethanolic extract in rats were done. In acute toxicity test, 4 groups of rats (n = 6/group: 3 males and 3 females) were chosen and the first control group received tap water, while the other three groups received Av seed ethanolic extract dissolved in tap water at doses of 150, 300, and 600 mg/kg, and general behavior, adverse effects, and mortality were recorded for up to 14 days. In subacute toxicity study, 72 rats (36 males and 36 females) were divided into 4 major groups; group I received tap water (control group), while animals in groups II, III, and IV (test groups) received oral intake of Av seed ethanolic extract dissolved in tap water at doses of 150, 300 and 600 mg/ kg bwt, respectively. Each of this major group was subdivided consequently into 3 subgroups (n = 6/group: 3 males and 3 females) where brain tissue, blood sample, body and organs weights were recorded at the beginning and then after two and four weeks of the experiment for the determination of hematological, biochemical and histopathological changes in tissues (liver, kidney, brain, spleen, heart, testis and ovary). With regard to acute toxicity, Av seed ethanolic extract did not induce any toxic effects or death or any organ toxicity. In subacute toxicity study; oral intake with Av seed ethanolic extract did not reveal any change in body and organs weights, hematological parameters, serum glucose and cholesterol, brain neurotransmitters, liver and kidney functions, male and female hormones. In conclusion, Av seed ethanolic extract is nontoxic to liver, kidney, brain, spleen, heart, testis and ovary.

Antidiarrheal and protein conservative activities of Psidium guajava in diarrheal rats.

OBJECTIVE: Psidium guajava occurs worldwide in tropical and subtropical areas. It has been used to treat inflammation, diabetes, fever, hypertension and ulcers. However, its antidiarrheal and protein conservative activities still need to be investigated. METHODS: Fifty-four male rats were divided into normal and diarrheal rats. The normal rats were divided into 4 groups: control, low-dose P. guajava leaf extract (50 mg/kg), high-dose P. guajava leaf extract (100 mg/kg) and gallic acid. Treatments were administrated orally in 1 mL saline for a 1-month period. The diarrheal rats were divided into 5 groups: desmopressin (0.2 mg/kg) drug, low-dose P. guajava leaf extract (50 mg/kg), high-dose P. guajava leaf extract (100 mg/kg), gallic acid and an untreated control. Doses were given daily for a 1-month period while the untreated control received no treatment. RESULTS: Diarrhea was responsible for an observed decline in kidney weight and serum sodium, potassium and chloride. Further, diarrhea was positively correlated with a significant increase in urine volume, and excretion of electrolytes, serum urea, creatinine and uric acid in the urine. In contrast, there was a proportional increase in the lipid peroxidation value in diarrhea and a significant decline was observed in serum superoxide dismutase, glutathione peroxidase and glutathione levels in diarrhea. Also, diarrhea inhibited blood proteins. The oral intake of P. guajava leaf extract by diarrheal rats restored all of these parameters to near normal levels. High-dose P. guajava leaf extract was more effective than the same compound at a low dose. CONCLUSION: P. guajava leaf extract elicited antidiarrheal and protein conservative effects.

Antidiarrheal and protein conservative activities of Psidium guajava in diarrheal rats / 中西医结合学报

OBJECTIVE@#Psidium guajava occurs worldwide in tropical and subtropical areas. It has been used to treat inflammation, diabetes, fever, hypertension and ulcers. However, its antidiarrheal and protein conservative activities still need to be investigated.@*METHODS@#Fifty-four male rats were divided into normal and diarrheal rats. The normal rats were divided into 4 groups: control, low-dose P. guajava leaf extract (50 mg/kg), high-dose P. guajava leaf extract (100 mg/kg) and gallic acid. Treatments were administrated orally in 1 mL saline for a 1-month period. The diarrheal rats were divided into 5 groups: desmopressin (0.2 mg/kg) drug, low-dose P. guajava leaf extract (50 mg/kg), high-dose P. guajava leaf extract (100 mg/kg), gallic acid and an untreated control. Doses were given daily for a 1-month period while the untreated control received no treatment.@*RESULTS@#Diarrhea was responsible for an observed decline in kidney weight and serum sodium, potassium and chloride. Further, diarrhea was positively correlated with a significant increase in urine volume, and excretion of electrolytes, serum urea, creatinine and uric acid in the urine. In contrast, there was a proportional increase in the lipid peroxidation value in diarrhea and a significant decline was observed in serum superoxide dismutase, glutathione peroxidase and glutathione levels in diarrhea. Also, diarrhea inhibited blood proteins. The oral intake of P. guajava leaf extract by diarrheal rats restored all of these parameters to near normal levels. High-dose P. guajava leaf extract was more effective than the same compound at a low dose.@*CONCLUSION@#P. guajava leaf extract elicited antidiarrheal and protein conservative effects.

The Role of Chlorogenic Acid Supplementation in Anemia and Mineral Disturbances Induced by 4-Tert-Octylphenol Toxicity.

4-tert-octylphenol (OP) is an endocrine-disrupting chemical that causes harmful effects to human health. Chlorogenic acid is the major dietary polyphenol present in various foods and beverages. The aim of the present study was to evaluate the protective role of chlorogenic acid in anemia and mineral disturbance occurring in OP toxicity in rats. Thirty-two male albino rats were divided into four equal groups (8 rats/group) as follows. The first (control) group was treated daily with an oral dose of 1 ml saline for two weeks. The second group was treated daily with an oral dose of 60 mg chlorogenic acid/kg body weight for two weeks. The third and fourth groups received daily intraperitoneal (ip) injections with 100 mg OP/kg body weight for two weeks; the fourth group was treated daily with an oral dose of 60 mg chlorogenic acid/kg body weight for three weeks starting one week before OP injections. The results revealed that OP induced significant decreases in hemoglobin, hematocrit, red blood cells, mean cell volume, mean cell hemoglobin, mean cell hemoglobin concentration, platelet count, white blood cells, lymphocyte and neutrophil percent, transferrin receptor, serum calcium, phosphorous, sodium, potassium, chloride, glutathione-S-transferase, glutathione peroxidase, catalase, glutathione reductase, and superoxide dismutase. Moreover, significant increases in serum hepcidin, ferritin, transferrin, erythropoietin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, urea, creatinine, selenium, zinc, manganese, copper, iron, malondialdehyde, and protein carbonyl levels were found in OP groups. OP exposure also induced cell apoptosis. Chlorogenic acid pretreatment in OP-treated groups restored all the mentioned parameters to approach the normal values. In conclusion, chlorogenic acid protects from anemia and mineral disturbances in 4-tert-octylphenol toxicity by ameliorating oxidative stress and apoptosis.

Role of caftaric acid in lead-associated nephrotoxicity in rats via antidiuretic, antioxidant and anti-apoptotic activities.

Background Lead is a toxic metal that is widely distributed in the environment where caftaric acid (CA) is the ester form of caffeic acid where CA is the major dietary polyphenol present in various foods and beverages. The aim of this study was to evaluate the effect of CA in lead acetate (LA)-associated nephrotoxicity through antidiuretic, antioxidant and anti-apoptotic activities. Methods Forty-eight male albino rats divided into six equal groups; group 1 control injected intraperitoneally (ip) with saline (1 mL/kg of bw) over two weeks period, group 2 injected ip with CA (80 mg/kg of bw) over two weeks period, groups 3, 4, 5 and 6 injected ip with 100 µmol/kg of bw LA over two weeks period where groups 4, 5 & 6 co-injected ip with 1-deamino-8-D-arginine vasopressin (dDAVP) drug (1 mg/kg of bw), CA (40 mg/kg of bw), and CA (80 mg/kg of bw), respectively. Results The results obtained revealed that LA induced a significant decrease in kidney weight and serum sodium, potassium and chloride, but caused a significant increase in urinary volume, urinary excretion of sodium, potassium and chloride, serum urea, creatinine and uric acid. The LA also caused a significant decrease in kidney superoxide dismutase, glutathione peroxidase and induced a significant decrease in glutathione level while caused an increase in lipid peroxidation level. In addition, LA caused a decrease in p53 expression while induced an increase in bcl-2 expression in the kidney tissues. Co-injection of CA to LA-treated group restored all the above parameters to approach the normal values. The results supported with histopathological examinations. Conclusions In conclusion, the effect of CA on LA-related nephrotoxicity was occurred through antidiuretic, antioxidant, anti-apoptotic activities where the effect of CA was dose dependent.

Supplementation of α-Tocopherol Attenuates Minerals Disturbance, Oxidative Stress and Apoptosis Occurring in Favism.

The favism is a metabolic disease that characterized with an acute hemolytic anemia where α-tocopherol is a type of tocopherol accumulated inside the human body. The objective of such a study was established to evaluate the effect of α-tocopherol in favism disorders. A total of 75 human cases were divided into 5 groups as follow; group 1 normal cases without any treatment and group 2 normal cases orally administrated α-tocopherol (200 mg/kg) once a day over 30 days period. Group 3 favism patients without any treatment. Groups 4 and 5 favism patients orally administrated 100 and 200 mg α-tocopherol/kg, respectively once a day over 30 days period. The results obtained revealed that oral administration of α-tocopherol into normal cases over 30 days period did not induce any biological change. In favism, hemoglobin, hematocrit, red and white blood cells, serum glucose, glucose-6-phosphate dehydrogenase, total protein, albumin, globulin, aspartate and alanine aminotransferases, blood glutathione, superoxide dismutase, glutathione peroxidase and serum calcium, phosphorous, sodium, potassium and chloride levels were significantly decreased. On the other hand, serum alkaline phosphatase, bilirubin, selenium, zinc, manganese, copper and iron, malondialdehyde levels showed significant increase in favism. Supplementation with α-tocopherol into favism restores all the above mentioned parameters to approach the normal levels. Also, α-tocopherol has anti-apoptotic effect in favism. In conclusion, α-tocopherol attenuates minerals disturbance, oxidative stress and apoptosis occurring in favism.