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The persistent and alarming rates of increase in cardiovascular and renal diseases caused by chemicals such as cobalt chloride (CoClForty-two male Wistar rats were randomly distributed to seven rats of six groups and classified into Group A (Control), Group B (300 part per million; ppm CoClCobalt chloride intoxication precipitated hypertension, renal damage, and oxidative stress. Immunohistochemistry revealed higher expression of angiotensin-converting enzyme (ACE) and podocin in rats administered only CoClTaken together, the antioxidant and metal-chelating action of Naringin administration against cobalt chloride-induced renal damage and hypertension could be through abrogation of angiotensin-converting enzyme and podocin signaling pathway.

Lead is one of the major pollutants that is harmful to both animals and humans. It is found in every aspect of the environment such as the air, water, and soil. This pollutant affects both wild and domestic birds. Naringin has an active principle called flavonoid that has been found to have medicinal properties, mostly because of its antioxidant and metal chelating properties. This study was carried out to investigate the protective effect of naringin as an antioxidant against lead-induced anemia, cardio and nephrotoxicity, and hypertension. This study also aimed at elucidating the use of naringin as a heavy metal binder in poultry feed. Thirty-six cockerel chicks were used for this study, and randomly grouped into six groups per group; group A served as the control, group B received Pb-only (300 ppm), group C (Pb and naringin; 80 mg/kg), group D (Pb and naringin; 160 mg/kg), group E (naringin 80 mg/kg), and group F (naringin 160 mg/kg), respectively, for 8 weeks. Lead (Pb) was administered via drinking water, while naringin was administered via oral gavage. Lead acetate intoxication precipitated anemia as indicated by significant reductions in the values of PCV, RBC, and Hb concentration in lead-treated chicks when compared with the controls. Also, lead administration induced hypertension together with increased oxidative stress, depletion of the antioxidant defense system, reduced nitric oxide production, and an increase in high blood pressure. Immunohistochemistry indicated high expressions of cardiac troponin, renal angiotensin-converting enzymes, and renal neutrophil gelatinase-associated lipocalin. Treatment with naringin corrected anemia, reduced oxidative stress, improved antioxidant system, reduced high blood pressure, and offered protection against lead acetate-induced cardio-renal dysfunction in cockerel chicks. We recommend that naringin should be incorporated poultry feeds as a metal binder.

Sodium fluoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil, and atmosphere. The persistent and alarming rate of increase in cardiovascular and renal diseases caused by chemicals such as NaF in mammalian tissues has led to the use of various drugs for the treatment of these diseases. The present study aimed at evaluating the renoprotective and antihypertensive effects of L-arginine against NaF-induced nephrotoxicity. Thirty male Wistar rats (150-180 g) were used in this study. The rats were randomly divided into five groups of six rats each as follows: Control, NaF (300 ppm), NaF + L-arginine (100 mg/kg), NaF + L-arginine (200 mg/kg), and NaF + lisinopril (10 mg/kg). Histopathological examination and immunohistochemistry of renal angiotensin-converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defense system, and blood pressure parameters were determined. L-arginine and lisinopril significantly (P 0.05) ameliorated the hypertensive effects of NaF. The systolic, diastolic, and mean arterial blood pressure of the treated groups were significantly (P 0.05) reduced compared with the hypertensive group. This finding was concurrent with significantly increased serum bioavailability of nitric oxide in the hypertensive rats treated with L-arginine and lisinopril. Also, there was a significant reduction in the level of blood urea nitrogen and creatinine of hypertensive rats treated with L-arginine and lisinopril. There was a significant (P 0.05) reduction in markers of oxidative stress such as malondialdehyde and protein carbonyl and concurrent increase in the levels of antioxidant enzymes in the kidney of hypertensive rats treated with L-arginine and lisinopril. The results of this study suggest that L-arginine and lisinopril normalized blood pressure, reduced oxidative stress, and the expression of renal ACE and mineralocorticoid receptor, and improved nitric oxide production. Thus, L-arginine holds promise as a potential therapy against hypertension and renal damage.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). This virus has become a global pandemic with unprecedented mortality and morbidity along with attendant financial and economic crises. Furthermore, COVID-19 can easily be transmitted regardless of religion, race, sex, or status. Globally, high hospitalization rates of COVID-19 patients have been reported, and billions of dollars have been spent to contain the pandemic. Angiotensin-converting enzyme (ACE) 2 is a receptor of SARS-CoV-2, which has a significant role in the entry of the virus into the host cell. ACE2 is highly expressed in the type II alveolar cells of the lungs, upper esophagus, stratified epithelial cells, and other tissues in the body. The diminished expressions of ACE2 have been associated with hypertension, arteriosclerosis, heart failure, chronic kidney disease, and immune system dysregulation. Overall, the potential drug candidates that could serve as ACE2 activators or enhance the expression of ACE2 in a disease state, such as COVID-19, hold considerable promise in mitigating the COVID-19 pandemic. This study reviews the therapeutic potential and pharmacological benefits of the novel ACE2 in the management of COVID-19 using search engines, such as Google, Scopus, PubMed, and PubMed Central.

Bisphenol A (BPA) is an environmental pollutant, a monomer used in the polymer industry to produce plastics. BPA has been reported to cause deleterious effects in both humans and animals. Naringin is one of the flavonoids with antioxidant and metal chelating properties. This study was carried out to assess the potential ameliorative effect of naringin on BPA-induced hepatotoxicity in cockerel chicks. Thirty-one-day old cockerel chicks used for this study were randomly divided into 6 groups of five chicks per group as follows: Group 1 (Control), Group 2 (BPA 100 mg/kg), Group 3 (BPA + 100 mg/kg naringin), Groups 4 (BPA + 200 mg/kg naringin), Group 5 (100 mg/kg naringin) and Group 6 (100 mg/kg naringin), respectively. The administration of BPA and naringin was through oral gavage. BPA intoxication precipitated significant (p 2O2 generation and MDA content with concomitant decrease in reduce glutathione, glutathione S-transferase, and superoxide dismutase activity in BPA intoxicated chicks. Histology revealed a moderate diffuse sinusoidal congestion, with a severe periportal cellular infiltration in BPA intoxicated chicks. Immunohistochemistry results revealed a higher expression of hepatic caspase 3 and TNF-α in chicks exposed to BPA alone relative to the control and chicks treated with naringin (100 mg/g and 200 mg/kg). Findings from this study showed that naringin administration restored hepatoxicity, improved antioxidant status, and lowered exaggerated values of cholesterol, oxidative stress indices, and ameliorated ultrastructure anarchy. Combining all, the incorporation of naringin into poultry feeds could position the flavonoid as a novel antioxidant and metal chelator with beneficial effects in the reduction of toxicities associated with environmental pollutants such as bisphenol A, thereby boosting production efficiency in livestock production.

Objectives Ovariectomy induces heightened response to vasoconstrictors, alters vasorelaxation and consequently causes hypertension due to increased oxidative stress in rats. Methods This study evaluated the ameliorative effects of ramipril and vitamin E, on primary haemodynamic parameters and cardiac antioxidant defence status, in ovariectomised rats using 64 adult female rats of the Wistar strain randomly divided as follows: Control (sham); Ovariectomised (OVX); OVX plus Ramipril; OVX plus vitamin E; and OVX plus Ramipril plus vitamin E. Results The plasma level of oestrogen was significantly lower (p2O2) generated decreased significantly (p Conclusions The supplementation of antihypertensive regimen with antioxidants such as vitamin E in the treatment of hypertension is therefore justifiable especially in ovariectomised or hypogonadal patients.

The medicinal application of sandpaper leaves in the management of hypertension has been reported with very little knowledge on the variety with better anti-hypertensive properties. Hence, this study seeks to compare phenolic content and the effect of some varieties of sand paper leaves (Ficus spp.), namely, Ficus exasperata (FE), Ficus asperifolia (FA), Ficus mucuso (FM) and Ficus capensis (FC) on the systolic and diastolic bood pressures (SBP and DBP), angiotensin-1-converting enzyme (ACE), and arginase activities and antioxidant status in L-NAME induced hypertensive rats. The animals were divided into eleven groups (n = 6): normotensive control rats, hypertensive rats, hypertensive rats treated with atenolol (10 mg/kg/day), hypertensive rats treated with 2.5% and 5% FE, FA, FM, and FC extract inclusive diet respectively. There was a significant rise (p < 0.05) in the systolic and diastolic blood pressures, ACE and arginase activities, and antioxidant status in the hypertensive rats. However, there were reductions in the SBP, DBP, ACE, and arginase activities and increase in the antioxidant status of the rats fed with the Ficus leaves. FM had the highest phenolic (91.09 mg/100 g) and flavonoid content (43.35 mg/100 g). FA showed the best anti-oxidant property, while FC showed the strongest inhibition of ACE and arginase activities.

Objectives Increasing hypertension incidence in Sub-Sahara Africa and the current cost of management of the metabolic disorder has necessitated research on medicinal plants employed in African Traditional Medicine for hypertension. Thus, this study evaluated antihypertensive effect of Annona muricata leaves or Curcuma longa rhizomes in experimentally-induced hypertensive male Wistar rats (n=70) which were unilaterally nephrectomized and daily loaded with 1% salt. Cardiovascular and haematological changes, as well as urinalysis were determined. Methods Rats were uninephrectomized and NaCl (1%) included in drinking water for 42 days. Extract-treated hypertensive rats were compared to normotensive, untreated hypertensive and hypertensive rats treated with lisinopril (5 mg/70 kg) or hydrochlorothiazide (12.5 mg/70 kg). A. muricata extract or C. longa extract were administered at 100, 200 or 400 mg/kg. Blood pressure (systolic, diastolic and mean arterial) and electrocardiogram was measured on day 41. Twenty-four-hour urine samples were collected from day 42. Blood samples were collected on day 43 for haematology (PCV, red cell indices, WBC and its differentials, and platelets). Results A. muricata or C. longa extracts caused a decline in elevated blood pressure of hypertensive rats. Heart rate and QT segment reduction coupled with prolonged QRS duration were reversed in extract-treated rats, with significant increases in hemogram parameters indicating increased blood viscosity. Also, leukocyturia, proteinuria and ketonuria with increased urine alkalinity, urobilinogen and specific gravity which are classical indicators of poor prognostic outcomes in hypertension were reversed in extract-treated rats. Conclusions In conclusion, A. muricata and C. longa have cardioprotective effect with reversal of derangements in haemogram and urinalysis associated with hypertension.

Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating fluoride-induced hypertension and nephrotoxicity with clofibrate, a peroxisome proliferator-activated receptor-alpha (PPARα) agonist. For this study, forty male Wistar rats were used and randomly grouped into ten rats per group, control, sodium fluoride (NaF; 300 ppm) only, NaF plus clofibrate (250 mg/kg) and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. The administration of NaF was by drinking water ad libitum, while clofibrate and lisinopril were administered by oral gavage. Administration of NaF induced hypertension, and was accompanied with exaggerated oxidative stress; depletion of antioxidant defence system; reduced nitric oxide production; increased systolic, diastolic and mean arterial pressure; activation of angiotensin-converting enzyme activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); and testicular apoptosis. Treatment of rats with clofibrate reduced oxidative stress, improved antioxidant status, lowered high blood pressure through the inhibition of angiotensin-converting enzyme activity, mineralocorticoid receptor over-activation, and abrogated testicular apoptosis. Taken together, clofibrate could offer exceptional therapeutic benefit in mitigating toxicity associated with sodium fluoride.

Petroleum exploration has continued to impact negatively the Niger Delta region of Nigeria. Oil spills from petroleum exploration contaminate both the aquatic and non- aquatic environments and destroy the ecosystem which makes people in these regions to be prone to diseases such as cancer, cardiovascular diseases, neurodegenerative disease, infertility, and sterility and also poverty. Some oxidative stress markers of the liver and muscle of fish (Clarias gariepinus) from Apata, Araromi, and Mahin rivers (located in the Niger Delta region) were compared with those of fish samples from a clean fish farm (control) in order to assess the level of pollution of the rivers. A significant increase in malondialdehyde level and myeloperoxidase (MPO) activity as well as alterations in antioxidant status (glutathione peroxidase, superoxide dismutase, reduced glutathione, and glutathione S-transferase) was observed in the organs of fish samples from Apata, Araromi, and Mahin rivers compared with the control. A significant increase in the frequency of micronucleated polychromatic erythrocytes (MnPCEs) was also observed in the fish samples from these rivers in comparison with the control. Based on results of our research, we can conclude that these rivers are polluted mainly by oil spillage and other industrial activities; therefore, the consumption of aquatic organisms from these rivers and the use of water from the rivers for domestic activities might be unsafe.

Cadmium (Cd) is one of the most dangerous heavy metals in the world. Globally, toxicities associated with cadmium and its attendant negative impact on humans and animals cannot be under-estimated. Cd is a heavy metal, and people are exposed to it through contaminated foods and smoking. Cd exerts its deleterious impacts on the testes (male reproductive system) by inducing oxidative stress, spermatogenic cells apoptosis, testicular inflammation, decreasing androgenic and sperm cell functions, disrupting ionic homeostasis, pathways and epigenetic gene regulation, damaging vascular endothelium and blood testes barrier. In association with other industrial by-products, Cd has been incriminated for the recent decline of male fertility rate seen in both man and animals. Understanding the processes involved in Cd-induced testicular toxicity is vital for the innovation of techniques that will help ameliorate infertility in males. In this review, we summed up recent studies on the processes of testicular toxicity and male infertility due to Cd exposure. Also, the usage of different compounds including phytochemicals, and plant extracts to manage Cd reprotoxicity will be reviewed.

Objectives This study aimed to explore the protective mechanism of caffeic acid (CAA) and chlorogenic acid (CHA) on cyclosporine (CSA) induced hypertensive rats. Methods Effect of CAA and CHA on diastolic blood pressure (DBP), mean arterial pressure (MAP), angiotensin-converting enzyme (ACE), e-nucleotide triphosphate dephosphorylase (e-NTPDase), 5′ nucleotidase and adenosine deaminase (ADA) activity in CSA-induced hypertensive rats were determined. Results CAA and CHA administration stabilized hypertensive effect caused by CSA administration. Also, altered activity of ACE (lung), e-NTPDase, 5′ nucleotidase, ADA as well as elevated malondiadehyde (MDA) level was restored in all the treated hypertensive rats in comparison with the untreated hypertensive rats. Conclusion Hence, these observed results could underlie some of the mechanisms through which CAA and CHA could offer antihypertensive effect.

Kidneys exposure to toxins can cause injuries, leading to their functional impairments. Traditionally, plants have been used for the treatment of renal disorders and numerous medicinal plants have been tested for their nephroprotective effects, in such cases as gentamicin (GM) and cisplatin (Cisp)-induced nephrotoxicity. This study assessed the ability of Acalypha wilkesiana’s extract to counteract its toxic effect based on the biochemical, histological and proinflammatory cytokines components in rats. Methods: Thirty-six male Wistar rats were randomly divided into nine groups (n=4 each) and administered the following treatments: a) normal control (1 mL/kg body weight normal saline from days 1-10); b) nephrotoxin (GM 120 mg/kg, days 2-7; or Cisp 7 mg/kg on day 3); c) standard drug (120 mg/kg Silymarin plus GM or Cisp, days 1-10); and, d) extract groups (100 or 250 mg/kg, days 1-10 plus GM). Blood samples were collected and subjected to hematological and biochemical evaluations while kidney tissue samples were examined for histopathological alterations, pro- and antioxidants, and expression of pro-inflammatory cytokines. Results: Treatment of the rats pre-exposed to GM or Cisp with the extract decreased the serum creatinine, urea and MDA levels. The GST and GPx levels were also restored in rats. Glomerular atrophy with tubular epithelial necrosis induced by either nephrotoxin was restored to near normal. The expression of COX-2 following the administration of either nephrotoxin was reversed after treatment with the extract. Conclusion: The A. wilkesiana extract exhibited significant nephroprotective property, which could potentially be regarded as a promising alternative to the management of renal diseases.%%%%This article is published in Iranian Journal of Toxicology and also available at : http://dx.doi.org/10.32598/ijt.14.4.658.1%%%%KNUST

Interest in medicinal plant research and usage has risen due to many reported side effects of synthetic drugs and their relatively higher cost. Ocimum americanum (family Lamiaceae) is a commonly used spice in Ghana with the aqueous extracts of leaves, flowers and stem been rich in saponins, alkaloids, flavonoids, and tannins. The aim of the study was to evaluate the nephroprotective potential of the aqueous extracts of O. americanum parts on gentamicin- and cisplatin-induced toxicity in rats. In a ten-day experiment, nephrotoxicity was induced with gentamicin (GM; 100 mg/kg b.wt. for 8 days) and cisplatin (Cisp; 6 mg/kg b.wt. for 1 day) after pre-treatment with 250 mg/kg b.wt. of the leaves, stem, and flower extracts of O. americanum and standard drug, silymarin (100 mg/kg b.wt.) for 10 days. The nephroprotective activity was evaluated by assaying the activity of serum kidney function parameter, kidney oxidative stress parameters, kidney inflammatory cytokines (NF-κB and IL-1) and histopathology. The activities of kidney function parameters of animals were significantly increased following Cisp and GM treatment with resultant alteration is kidney microarchitecture, over-expressions of NF-κB and IL1 and kidney oxidative stress markers. Extract pre-treatment restored kidney function to near-normal, downregulating the expressions of IL-1 and NF-κB and improved levels of reduced GSH contents, GPx and SOD activities. However, leaves extract showed the best protection against GM while all extracts showed improved protection (> 50%) against Cisp. Extract of Ocimum americanum exhibit nephroprotective activity and could be developed as a potent kidney protector.

Concerns over fluoride toxicity have increased in recent times due to high exposures from various anthropogenic sources such as industrial sites, fluoride-containing pesticides, drugs, dental products, refridgerants and fire extinguishers. There is, therefore, continued search for agents that could ameliorate the toxicity of this chemical in various body organs. In this study, we sought to investigate the protective effects of L-Arginine (L-Arg), a nitric oxide donor, on liver toxicity induced by sodium fluoride (NaF) in rats. Rats received NaF (300 mg L−1) in drinking water alone or in co-treatment with L-Arg at two different doses, 100 and 200 mg kg−1, by oral gavage, for 7 days. Markers of hepatotoxicity, oxidative stress and antioxidant status were thereafter assessed. NaF caused marked increase in serum transaminases: alanine aminotransferase, Aspartate aminotransferase and Alkaline phosphatase, along with atrophy of the centri-lobular hepatic cords and dilatation of the sinusoids. Moreover, NaF stimulated increases in hepatic contents of hydrogen peroxide (H2O2), nitric oxide (NO), protein carbonyls, malondialdehyde and advanced oxidation protein products. NaF also inhibited the activities of antioxidant enzymes, Glutathione peroxidase and Superoxide dismutase. However, L-Arg supplementation caused significant alleviation of NaF hepatotoxicity by reducing lipid and protein oxidation indices, stimulation of antioxidant systems along with increased production of NO. L-Arg showed promise as a potential protective agent against NaF-induced hepatotoxicity via restoration of oxidant-antioxidant balance. Further studies are required to understand the involvement of NO signaling in the protective effects of L-Arg against fluoride toxicity.

Objectives Hypertension is the number one risk factor and primary contributor of cardiovascular diseases. Caesalpinia benthamiana is a valuable medicinal plant with unvalidated anti-hypertensive activity. This study was carried out to explore the antihypertensive effect of C. benthamiana on uninephrectomized hypertensive rats. Methods Fifty rats were grouped into five groups, each containing 10 animals: Group A-normal control (normotensive); B-uninephrectomized control; C-uninephrectomized treated with 50 mg/kg C. benthamiana extract; D-uninephrectomized treated with 100 mg/kg C. benthamiana; and E- uninephrectomized treated with 10 mg/kg of Lisinopril. Results Significant increases were observed in systolic, diastolic and mean blood pressure of uninephrectomized control rats. Furthermore, markers of oxidative stress (malondialdehyde, hydrogen peroxide, protein carbonyl, myeloperoxidase and the advanced oxidative protein products) increased significantly while antioxidant status (reduced glutathione, glutathione peroxidase, glutathione S-transferase and superoxide dismutase), reduced significantly in uninephrectomized hypertensive rats. Histopathology revealed thrombosis and occlusion of coronary vessels in the heart, and congestion in the kidney. However, the observed high blood pressure parameters were remarkably normalized together with reduction in markers of oxidative stress and improvement in antioxidant defence system of uninephrectomized hypertensive rats treated with C. benthamiana extract similar to normotensive rats. Conclusions C. benthamiana extract exhibited antihypertensive action, strong antioxidant ability, attenuated oxidative stress-mediated hypertension and lessened the development of cardiac and renal damage associated with hypertension induced by uninephrectomy and high dietary intake of salt. Together, C. benthamiana extract might be useful in the management of hypertension due to volume overload in the cardiovascular system.

Hypertension is an important risk factor for cardiovascular diseases, which are major causes of mortality globally. This study evaluated the antihypertensive effects of Harungana madagascariensis on sodium fluorideinduced hypertension. Twenty-five rats were randomly divided into five groups (A-E). Group A (control), received normal food and water with no treatment; Groups B to E were exposed to 300 ppm sodium fluoride (NaF). In addition, Group C was treated with 10 mg/kg enalapril, while Groups D and E were treated with 100 mg/kg and 200 mg/kg of H. madagascariensis extract, respectively. The result showed that there was a significant decrease in the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) of the rats treated with 200 mg/kg of H. madagascariensis compared with rats exposed to NaF alone. Also significant increase was observed in the activities of the enzymatic and non-enzymatic antioxidants in the cardiac and renal tissues of rats treated with 100 mg/kg and 200 mg/kg of H. madagascariensis extract similar to enalapril, compared with rats exposed to NaF alone. However, serum nitric oxide (NO) decreased significantly in rats exposed to NaF alone compared with rats that received 200 mg/kg H. madagascariensis as treatment. Blood urea nitrogen (BUN) and creatinine increased significantly in rats exposed to NaF alone compared with rats that received 200 mg/kg H. madagascariensis as treatment. The histopathology of the cardiac tissue of the rat exposed to NaF alone showed mild hydropic and vacuolar degeneration of cardiomyocytes, while the renal tissue showed foci of markedly flattened tubular epithelial cells and congestion of interstitial blood vessels. The aforementioned lesions were ameliorated in rats treated with 200 mg/kg H. Madagascariensis. In conclusion, H. madagascariensis had potent antihypertensive effect in rats. The effect was probably mediated via the alleviation of oxidative stress in cardiac and renal tissues. Key words: Harungana madagascariensis, Antioxidant activity, Oxidative Stress, Hypotensive effect, Sodium fluoride.

Background and Aim: Momordica charantia is a highly valued plant, widely distributed in the tropical and subtropical regions. The plant is reported to have a wide range of medicinal uses. This study was designed to explore the ameliorative potential of M. charantia methanol leaf extract in alloxan-induced diabetic animal model with a particular focus on the liver. Materials and Methods: Hepatoprotective effect of methanol leaf extract of M. charantia was assessed in alloxan-induced toxicity in 50 rats divided into five groups (A-E) (n=10). Group A normal control, Group B was toxicant group, and Group C animals received glibenclamide treatment while Groups D and E received extracts at 200 and 400 mg/kg doses, respectively. The experiment lasted for 28 days. Histopathological changes, blood glucose level, and serum enzymes such as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, oxidative status and caspase-9, and interleukin-1β (IL-1β) were evaluated. Results: Extract-treatment caused a decreased blood glucose level, markers of oxidative stress such as malondialdehyde and hydrogen peroxide (H2O2). Treatment of rats with leaf extract of M. charantia resulted in increased levels and activities of protein thiols, non-protein thiols, glutathione (GSH), glutathione peroxidase, glutathione S-transferase, and superoxide dismutase indicating its antioxidant potential. The liver section revealed mild distortion of the hepatic architecture compared to the toxicant group, while decreased expressions of caspase-9 and IL-1β in extract-treated groups was observed. Conclusion: The plant extract exhibited antioxidant, anti-apoptotic, and anti-inflammatory effects, thus showing its hepatoprotective property.

Liver diseases have continued to be a major health problem in the world’s population with drug-induced liver damage as one of the causes. Tecoma stans (L.) Juss. ex Kunth is an ornamental plant and almost all parts of this plant are of medicinal importance. It exhibits strong antioxidant, anti-inflammatory, antispasmodic, and wound healing activities. This study was conducted to assess the hepatoprotective effects of hydroethanolic extract of Tecoma stans (TSE) against acetaminophen- and CCl4-induced liver damage in rats. CCl4 (1 ml/kg body weight dissolved in olive oil) and acetaminophen (500 mg/kg b.wt) was used to induce hepatotoxicity in the animals. Animals were treated with TSE (dose: 100 mg/kg and 250 mg/kg b.wt) and standard drug, silymarin (100 mg/kg), for 7 days. Biochemical parameters such as ALT, AST, ALP, bilirubin (total and indirect), serum proteins (total protein, album and globulin), total cholesterol and triglycerides, creatinine and urea were evaluated. Also, liver histology and oxidative stress assessment were conducted. Significant increases in the major indicators of liver toxicity were observed in the paracetamol and CCl4 only group when compared to the normal. Levels of these biochemical parameters were reduced after the administration TSE (250 mg/kg) and the silymarin (100 mg/kg). The biochemical assessment was supported by histological observations. TSE has shown to possess significant hepatoprotective and antioxidant properties in the current study.

Introduction: Liver fibrosis is one of the most common clinical manifestations of hepatic diseases. However, though many synthetic drugs exist for the treatment and prevention of liver diseases, liver injuries still persist. The present study, therefore, sought to investigate the subacute protective effects of Acalphya wilkesiana against carbon tetrachloride (CCl4)-induced toxicity in animals. Methodology: Liver injury was induced in experimental animals by administering CCl4 (1:1 v/v in olive oil, intraperitoneally (i.p.), twice weekly for 8 weeks) after pre-treatment with extract of A. wilkesiana (AWE). AWE (250 mg/kg) and Silymarin (120 mg/kg) were administered orally (daily for 8 weeks). The hepatoprotective effect was studied by assaying the activity of liver enzymes, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alpha-fetoprotein. The effect of the treatments on liver prooxidants (e.g. malondialdehyde [MDA]) and antioxidants (e.g. superoxide dismutase [SOD], reduced glutathione [GSH], glutathione peroxidase [GPx], and glutathione transferase [GST]), as well as inflammatory cytokines (e.g. interleukin [IL]-17, IL-23, nuclear factor kappa beta [NF-kB], and cycloxygenase-1 [COX-1]) and the histology of the liver were also examined. Results: The activity of liver function biomarkers changed significantly upon CCl4 administration; increases in ALT, total and direct bilirubin, and some fibrosis indices (e.g. alpha-fetoprotein and APRI [p

Background and Aim: High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats. Materials and Methods: The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), Group D was fed with cocoa-feed compounded with 8% salt for 4 weeks after uninephrectomy, and Group E was uninephrectomized rats on a normal diet. The left kidneys of animals in Groups C, D, and E were removed by surgery. After 4 weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues. Results: Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress. Conclusion: These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.

Murraya koenigii (L.) Spreng. (Rutaceae) has been reported to positively affect liver function. However, the effect of M. koenigii leaves on NTwo variants of curry tea were formulated; one was formulated entirely from leaves of M. koenigii, the other was formulated with thaumatin-rich aril obtained from seeds of Thaumatococcus danielii (Benn.) Benth. (Marantaceae). Group I animals served as control and were untreated. Groups II and V animals were administered curry tea (CT). Group III and VI animals received curry-thaumatin tea (CTT). Concurrently, L-NAME (40 mg/kg) was administered to groups IV-VI respectively for 21 days. Blood and liver samples were collected at the end of the study for biochemical, histological, and immunohistochemical analysis.L-NAME induced liver dysfunction evidenced by liver histology, increased activities of ALT, AST, hyperlipidemia, hepatic oxidative stress and increased hepatic NF-kB expression. Administration of CT and CTT ameliorated the L-NAME induced liver dysfunction evidenced by liver histology, increased NO hepatic bioavailability, reduced activity of ALT and AST, increased hepatic antioxidant system and decreased hepatic NF-kB expression. Thaumatin taste/flavor enhancer did not significantly reduce or potentiate the hepatoprotective, antioxidant and anti-lipidemic property of aqueous curry tea extracts in rats.L-NAME impaired liver function in rats. CT and CTT interfered with the ability of L-NAME to inhibit NO synthesis which was associated with ameliorated hepatic dysfunction.The study reports that non-selective inhibition of nitric oxide by L-NAME in rats impairs liver function and formulated curry tea types interfered with the ability of L-NAME to inhibit NO synthesis which was associated with ameliorated hepatic dysfunction in rats.

This study was designed to investigate the modulatory role of Luteolin (Lut) on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT2R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT2R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p2R and MCR was high in the Dcf and Dcf+NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls) with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, which was significantly ameliorated in Lut-treated rats. The protective effect of Lut on blood pressure was probably mediated by stimulation of renal expressions of AT2R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.

Sodium fluoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil and the atmosphere. The persistent and alarming rate of increase in cardiovascular and renal diseases and disorders caused by chemicals such as sodium fluoride (NaF) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the renoprotective and antihypertensive effects of L- Arginine on NaF-induced nephrotoxicity. Thirty male Wistar rats (150 – 180 g) were used in this study. The rats were randomly divided into five groups of six rats each as Control, NaF (300 ppm), NaF + L- Arginine (100 mg/kg), NaF + L- Arginine (200 mg/kg), and NaF + Lisinopril (10 mg/kg), respectively; orally for eight days. Histopathological examination and immunohistochemistry of renal angiotensin converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defence system, and blood pressure parameters were determined. L- Arginine significantly (p hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl (PCO) and concurrent increase in the levels of antioxidant enzymes in the kidney of hypertensive rats treated with L arginine. The results of this study suggest that L- Arginine normalized high blood pressure, reduced oxidative stress, reduced the expression of renal ACE and MCR, and improved nitric oxide production. Thus, L- Arginine holds promise as a potential therapy against hypertension and renal damage.

Lead is one of the major pollutants in the world which is deleterious to both animals and humans. It is found in every aspect of the environment such as the air, water and soil. This pollutant affect both wild and domestic birds. Naringin is a flavonoid that has been found to have medicinal properties mostly because of its antioxidant and metal chelating effects. This study was carried out to investigate the protective effect of naringin against lead-induced anaemia, cardio and nephrotoxicity, oxidative stress, and hypertension. Thirty -six cockerel chicks were used for this study, and randomly grouped into six chicks per group; Group A served as the control, Group B received Pb only (300 ppm), Group C (Pb and naringin; 80 mg/kg), Group D (Pb and naringin; 160 mg/kg), Group E (naringin 80 mg/kg) and Group F (naringin 160 mg/kg), respectively for eight weeks. Lead (Pb) was administered via drinking water while Naringin was administered via oral gavage. Lead acetate intoxication precipitated anaemia as indicated by significant reductions in the values of PCV, RBC, and Hb concentration in lead-treated chicks when compared with the controls. Also, lead administration induced hypertension together with increased oxidative stress, depletion of the antioxidant defense system, reduced nitric oxide production and increase in high blood pressure. Immunohistochemistry indicated high expressions of cardiac troponin, renal angiotensin converting enzymes, and renal neutrophil gelatinase associated lipocalin. Treatment with naringin corrected anemia, reduced oxidative stress, improved antioxidant system, reduced high blood pressure, and offered protection against lead acetate-induced cardio-renal dysfunction in cockerel chicks.

Fluoride is an environmental contaminant that is ubiquitously present in air, water, and soil. It is commonly added in minute quantity to drinking water, toothpaste, and mouth rinses to prevent tooth decay. Epidemiological findings have demonstrated that exposure to fluoride induced neurodevelopmental toxicity, developmental neurotoxicity, and motor disorders. The neuroprotective effect of clofibrate, a peroxisome proliferator-activated receptor alpha agonist, was investigated in the present study. Forty male Wistar rats were used for this study and randomly grouped into 10 rats per group as control, sodium fluoride (NaF) alone (300 ppm), NaF plus clofibrate (250 mg/kg), and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. NaF was administered in drinking water while clofibrate and lisinopril were administered by oral gavage. Markers of neuronal inflammation and oxidative stress, acetylcholinesterase activity, and neurobehavioral (hanging wire and open field) tests were performed. Immunohistochemistry was performed on brain tissues, and they were probed with glial fibrillary acidic protein, ionized calcium-binding adaptor molecule 1, and cerebellar Ca2+ -binding protein calbindin-D28k. The results showed that NaF significantly increased of oxidative stress and neuroinflammation and inhibited AChE activity. Immunostaining showed reactive astrocytes, microgliosis, loss of dendritic spines, and arborization in Purkinje cells in rats administered only NaF. Neurobehavioral results showed that cotreatment of NaF with clofibrate improved muscular strength and locomotion, reduced anxiety, and significantly reduced astrocytic count. Overall, cotreatment of NaF with either clofibrate or lisinopril showed neuroprotective effects by mitigating neuronal inflammation and oxidative and motor incoordination. Hence, clofibrate could be seen as a novel drug candidate against neurodegeneration and motor disorders.

Water pollution indices and oxidative stress biomarkers in African sharp-toothed catfish, Clarias gariepinus were used to evaluate the health status of Abereke River on the Ilaje coastal zone of Ondo’s Niger Delta region. Muscle and liver tissues from fishes harvested from the river and from a clean fish farm were comparatively subjected to heavy metal status and redox stress biomarker analyses. Water samples from the river and fish farm were also subjected to water quality tests. Our findings showed significant elevations in bacterial contaminants, heavy metal pollutants, and particulate matter deposits in Abereke River. In addition, heavy metal deposits were found in tissues of fish harvested from the river correlated with increases in markers of oxidative stress and depletions in antioxidant defense systems. Taken together, water from Abereke River is unsafe for human consumption, and consumption of aquatic organisms from the river may be harmful to health.

Nephrotoxicity is one of the most common kidney conditions. However, most conventional drugs are not adequate for treatment. This study was designed to evaluate the nephroprotective activity of 50% hydroethanolic leaf extract of Griffonia simplicifolia (DC.) Benth in drug-induced nephrotoxicity in Sprague–Dawley rats. Nephrotoxicity was induced in experimental animals by administering gentamicin and cisplatin after pre-treatment with hydroethanolic extract of G. simplicifolia (GSE). GSE at 100 and 250 mg/kg were administered for 7 and 10 days by oral gavage in the gentamicin and cisplatin models, respectively. Silymarin (120 mg/kg) was given as the standard nephroprotective drug. Nephroprotective effect was studied by assaying the activity of kidney function biomarkers such as creatinine, urea, sodium, chloride, and potassium concentrations. The effect of the treatments on kidney antioxidant enzymes (SOD, MDA, GSH, GPx, GST and NO), inflammatory cytokines (IL 17, IL 23 and COX-2) and the histology of the kidney were also examined. The activity of all the kidney function biomarkers changed significantly in gentamicin and cisplatin-treated rats; increased in urea and creatinine concentration and decreased in Na, K and Cl concentrations. Co-administration of GSE with the nephrotoxins restored these to normal levels. It also reduced NO concentration in both the gentamicin and cisplatin model and increased GPx concentration in the gentamicin model. GSE showed a higher percentage protection than silymarin, a standard nephroprotective drug, in both the gentamicin and cisplatin models. Intensity of structural alterations revealed that the GSE treatments have a protective potential against nephrotoxicity. GSE treatments improved expressions of IL17 and IL23, thus underscoring the proinflammatory and healing properties of GSE, respectively. The results generally indicate that leaves of G. simplicifolia possess nephroprotective activity.