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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 3  |  Page : 65-73

Methanolic leaf extract of Dryopteris dilatata reverses kidney injury on streptozotocin-induced diabetic male wistar rats


1 Department of Pharmacology, PAMO University of Medical Sciences, Port-Harcourt, Nigeria
2 Department of Human Physiology, Faculty of Basic Medical Sciences, College of Medicine, Enugu State University of Science and Technology, Agbani, Enugu, Nigeria
3 Department of Experimental Pharmacology and Toxicology, University of Port-Harcourt, Choba, Rivers State, Nigeria
4 Department of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, Enugu State University of Science and Technology, Agbani, Enugu, Nigeria

Date of Submission31-Jul-2022
Date of Acceptance13-Sep-2022
Date of Web Publication05-Dec-2022

Correspondence Address:
Dr. Celestine Okafor Ani
Department of Human Physiology, Faculty of Basic Medical Sciences, College of Medicine, Enugu State University of Science and Technology, Enugu
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njecp.njecp_10_22

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  Abstract 

Background: Hyperglycemia when sustained leads to diabetes which has become a chronic disorder having morbidity and mortality rate. This study investigated the effect of methanolic leaf extract of Dryoptersis dilatata (MEDd) on kidney injury caused on streptozotocin (STZ)-induced diabetic Wistar rats. Materials and Methods: Thirty Wistar rats were divided into five groups of six rats each. Group 1 received distilled water (10 ml/kg); Group 2 received STZ (60 mg/kg) only, Groups 3 and 4 received STZ followed by 400 and 800 mg/kg of MEDd, respectively, while Group 5 received STZ + Pioglitazone (10 mg/kg). After 2 weeks of treatment, rats were sacrificed and blood, spleen, liver, pancreas, and kidney were collected for biochemical analysis. Results: The results showed that MEDd extract caused a significant decrease (P < 0.05) in STZ-induced diabetic rats, oxidative stress markers, malondialdehyde nitric oxide, and glutathione superoxide were ameliorated in organs such as the kidney and pancreas in diabetic rats after treatment with MEDd. Kidney markers (urea and creatinine) were ameliorated as well as reduction in organ weights in diabetic rats following treatment with MEDd. Conclusion: Therefore, it was observed from our study that MEDd has antidiabetic and nephron-protective capacity as it ameliorates in vivo adopted in lieu of nephropancreatic caused by STZ-induced diabetes.

Keywords: Antioxidants, diabetes mellitus, Dryopteris dilatata, kidney injury, Streptozotocin


How to cite this article:
Ajirioghene AE, Ani CO, Ajebor DN, Elavieniso AF, Okolo KO. Methanolic leaf extract of Dryopteris dilatata reverses kidney injury on streptozotocin-induced diabetic male wistar rats. Niger J Exp Clin Biosci 2022;10:65-73

How to cite this URL:
Ajirioghene AE, Ani CO, Ajebor DN, Elavieniso AF, Okolo KO. Methanolic leaf extract of Dryopteris dilatata reverses kidney injury on streptozotocin-induced diabetic male wistar rats. Niger J Exp Clin Biosci [serial online] 2022 [cited 2023 Feb 9];10:65-73. Available from: https://www.njecbonline.org/text.asp?2022/10/3/65/362644


  Introduction Top


Diabetes mellitus (DM) is a chronic metabolic disorder that is caused by insufficiency in insulin secreted by the pancreas, insulin resistance or the ineffectiveness of the insulin produced and in some cases both, DM can be inherited or acquired. Diabetes is a killer disease that affects millions of people and is the second leading cause of blindness and renal diseases in the world, it is mainly characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism and is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels.[1] This deleterious complication has made the prevalence of diabetes increased over the past few decades in different parts of the world. The most recent data from the International Diabetes Federation indicated that an estimated 415 million adults aged 20–79 years worldwide have DM in 2015 and the number will project to 642 million in 2040, with the prevalence increasing from 8.8% to 10.4%. Regionally, the age-adjusted prevalence of DM is 3.8% in Africa, 7.3% in Europe, 10.7% in Middle East and North Africa, 11.5% in North America and Caribbean, 9.6% in South and Central America, 9.1% in Southeast Asia, and 8.8% in Western Pacific. China, India, and the USA remain the top three countries with the largest number of people with DM.[2]

DM as metabolic disorder can be caused by the autoimmune destruction or annihilation of the pancreatic-β cells with no insulin production which is seen in Type 1 DM also known as insulin-dependent DM. Patients with Type 1 DM are prone to ketoacidosis and need daily administration of insulin to control the amount of glucose in their blood and it occurs in children and adolescents. Diabetes can also be due to insufficient production of insulin or desensitization of insulin receptors that precludes the entry of glucose into the cell which is classified as Type 2 DM and it accounts for the vast majority of people with diabetes around the world.[3]

Symptoms of diabetes includes but is not limited to, excessive thirst (polydipsia); excessive urination (polyuria) and dehydration; excessive hunger or appetite (polyphagia); unexplained weight loss, blurred vision, nearsightedness, or other vision problems; frequent infections, including skin infections, thrush, gingivitis, urinary tract infections, and yeast infections; slow healing of sores; skin problems, such as itchiness or acanthosis.[4]

Long-term effects of DM on organs can lead to complications such as nephropathy which leads to renal failure, retinopathy with potential loss of vision. Also included is peripheral nephropathy which might result in foot ulcers, Charcot joints and amputations, hypertension, and sexual dysfunction.[5] Prolonged hyperglycemia and hyperlipidemia in DM can lead to oxidative stress as a result of reactive oxygen species overproduction in the cytosol or mitochondria, which counteracts the cellular redox balance and induces more oxidative stress. Glucose toxicity in β cells in DM is a significant cause of oxidative stress, as high glucose exposure increases oxidative stress in human islets and pancreatic β-cell lines and as pancreatic β-cell function gradually worsens, hyperglycemia becomes apparent.[6]

Several disadvantages related to the use of oral hypoglycemic agents have been reported which includes reduction of effciency (drug resistance), like in the case of sulfonylureas that lose their effectiveness after 6 years of treatment in approximately 44% of patients, whereas glucose-lowering drugs have been reported of not being able to control hyperlipidemia and also adverse effects such as flatulence, hypoglycemia, myalgia, mild skin rash, diarrhea, constipation, swelling of extremities, osteoarthritis, lactic acidosis (rare cases), and even toxicity has been identified with the use of synthetic drugs.[7]

The use of natural compounds in animal DM models has been shown to improve glycogenic control, reduce inflammation, decrease oxidative stress and neurodegeneration, and prevent various complications of DM. Natural polyphenols are secondary metabolites of plants and found largely in fruits; vegetables. Polyphenols are, therefore, considered the most abundant antioxidants in the human diet, and diets rich in polyphenols provide protective effects against DM, cardiovascular diseases, cancer, and several neurodegenerative diseases. The administration of resveratrol which is a natural polyphenol compound, widely found in grapes and blueberries, in streptozotocin (STZ)-NA-induced DM type 2 rats decreased blood glucose and glycosylated hemoglobin levels and increased the antioxidant activity of superoxide dismutase, catalase, and glutathione (GSH) peroxidase in the liver.[7]

Medicinal plants have played an important role in the treatment of many diseases and are believed to be well appropriated with the human body and produce lesser side effects than the pharmaceuticals.[8]

Plants by the virtue of their diverse phytochemical constituents may provide more acceptable, cheaper and safer lead compounds with multimodal mechanisms of action in managing DM, presently medicinal plants of which one such plant is Dryopteris dilatata have played an important role in the treatment of DM under developed countries and proved their potency in alleviating diabetes and complications attributed to diabetes with little or no side effects compared to the several adverse effects associated with use of synthetic agent. Hence, this study investigated the reversal activity of methanolic leaf extract of D. dilatata on kidney injury on STZ-induced diabetic Wistar rats.


  Materials and Methods Top


Plant collection and identification

D. dilatata leaves were collected from a wide growing habitat within Olomoro in Isoko South Local Government Area of Delta State and was identified in the Department of Botany and Taxonomy Unit, Delta State University, Abraka, with a voucher specimen number; FHI 1100338. The leaves were washed and air dried at room temperature (25°C ± 97% humidity) and ground to fine powder and followed by the extraction using method of.[9]

Induction of experimental diabetes

Diabetes was induced following the method of Akpotu et al.[10] with a single intraperitoneal injection of STZ at 60 mg/kg in sterile citrate buffer (0.1 M, pH 4.5) to Wistar rats fasted overnight. Hyperglycemic level of the rats was confirmed after 72 h using glucometer and strips (ACCUCHEK® Active) and rats with blood glucose level of ≥200 mg/kg were selected for the study.

Animal procurement

Thirty male Wistar rats weighing between 150 g and 200 g were used for the study. The rats were purchased from the Animal House Unit of PAMO University of Medical Science, Port-Harcourt, Rivers State, Nigeria, and were kept under standard laboratory condition with 12 h light-dark cycle at 18°C–26°C and relative humidity of 30%–70%). The rats were fed with pelletinized rat chow with clean drinking water ad libitum and were acclimatized for 2 weeks before commencement of the study. Ethical approval was obtained from PAMO Research Ethics Committee; Animal handling was done in accordance with the guidelines established by the National Institute of Health for care and use of laboratory animals.

Experimental design

The animals were divided into five groups of six each.

  • Group 1 (Normal control): Fed with normal feed and water ad libitum
  • Group 2 (Diabetic control): Diabetic untreated group
  • Group 3 (high dose of the methanolic leaf extract of D. dilatata [MEDd]): diabetes + 800 mg/kg of MEDd extract
  • Group 4 (low dose of MEDd): diabetes + 400 mg/kg of MEDd extract
  • Group 5 (standard antidiabetic drug): Diabetes + 500 mg/kg of pioglitazone.


Sample collection

At the beginning of the experiment, the blood glucose levels of the rats were taken before and after induction of diabetes, after which their blood glucose levels were taking at every 7th day and 30 min' interval on the last day of the experiment. After 2 weeks, the animals were sacrificed, the kidney, liver, pancreas, and spleen was harvested, weighed, and homogenized for biochemical analysis. Serum and supernatant of homogenate were used for urea, creatinine, and antioxidant malondialdehyde (MDA, Nitrate, GHS) biomarkers using their respective kits.

Measurement of blood glucose level

Blood glucose level of the rats was measured on the 7th day for 2 weeks and a glucose tolerance test was done on the 14th day of the experiment after a post treatment with MEDd and glucose load of 2 mg/kg after which their glucose level was checked for intervals of 30, 60, 90, 120, and 150 min' duration with blood gotten from the tail vein of the rats and results recorded.[11]

Statistical analysis

Data collected were expressed as mean ± standard error of mean and analyzed using one-way analysis of variance and comparison of the groups was performed using post hoc Newman–Keuls test using GraphPad prism 7.0 (GraphPad software, San Diego, CA, USA). P < 0.05 was considered statistically significant.


  Results Top


Organ weight

[Figure 1] shows the organ (spleen, liver, and kidney) weight changes between normal control and treatment groups. There was no statistical (P > 0.05) significant difference between the spleen weight of the normal control and other treatment groups. There was a statistically significant increase between normal control and diabetic control group in the liver weight of normal control and other treatment groups, likewise a statistically significant (P < 0.05) decrease was seen in diabetic control group and other treatment groups). Furthermore, the kidney weight of normal control and other treatment groups showed a statistically significant (P < 0.05) increase between normal control and diabetic control groups; likewise a statistically significant decrease was seen between diabetic control group and other treatment groups.
Figure 1: Bar chart representation of organ (spleen, liver, and kidney) weight changes. #P < 0.05 statistically significant when compared with normal control group; *P < 0.05 statistically significant when compared with Diabetic Control group

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[Figure 2] shows the levels of kidney nitrite expression in the normal control and treatment groups. Across treatment groups, diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with normal control, there were notable increases which was not statistically (P > 0.05) significant. In addition, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there were notable decreases which were no statistically (P < 0.05) significant difference.
Figure 2: Bar chart representation of kidney nitrite levels

Click here to view


[Figure 3] shows the levels of kidney MDA expression in normal control and treatment groups. Across treatment groups, diabetic control revealed a statistically significant (P < 0.05) increase when compared with normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with normal control, there were notable decreases which was not statistically (P > 0.05) significant. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there was a statistically (P < 0.05) significant decrease.
Figure 3: Bar chart representation of kidney MDA Expression Levels. # (statistically significant when compared with normal control group); * (Statistically Significant when compared with diabetic control group) (P < 0.05), MDA: Malondialdehyde

Click here to view


[Figure 4] shows the levels of kidney GSH expression in normal control and treatment groups. The diabetic control revealed a statistical (P < 0.05) significant decrease when compared with normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with normal control, there were notable increases which was not statistically (P > 0.05) significant. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there was a statistically (P < 0.05) significant increase.
Figure 4: Bar chart representation of kidney glutathione (GSH) expression Level. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group). GSH: Glutathione

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[Figure 5] shows the result for glucose tolerance test in 30 min interval for 2.5 h At the 30th min assessment, the diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. A statistically (P < 0.05) significant decrease was observed between diabetic control group and other treatment groups except D + Pio (10 mg/kg), which showed an obvious reduction while at the 60th min assessment, the diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. A notable decrease was seen between diabetic control group and other treatment except D + Pio (10 mg/kg), which showed a statistically significant decrease. At the 90th min assessment, the diabetic control revealed a statistically significant increase when compared with normal control. A statistically significant decrease was seen between diabetic control group and other treatment, except D + Pio (10 mg/kg), which showed an obvious reduction. At the 120th min assessment, the diabetic controlled group revealed a statistically (P < 0.05) significant increase when compared with normal control. A notable decrease was seen between diabetic control group and other treatment groups except D + MEDd (800 mg/kg), which showed a statistically (P < 0.05) significant decrease. Finally, at the 150 min assessment, the diabetic control revealed a statistically significant (P < 0.05) increase when compared with normal control. A notable decrease was seen between diabetic control group and other treatment groups except D + Pio (10 mg/kg), which showed a statistically significant decrease.
Figure 5: Bar chart representation of glucose tolerance assessment in minutes (30, 60, 90, 120 and 150). #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

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[Figure 6] shows the assessment result for glucose tolerance in weeks. There was no statistically (P > 0.05) significant difference across groups, 0 and 72 h. Week 1 assessment of the glucose tolerance test showed that the diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. A statistically significant decrease was seen between diabetic control group and other treatment groups except D + MEDd (800 mg/kg), which showed a notable decrease. The week 2 assessment showed that the diabetic control revealed a statistical (P < 0.05) significant increase when compared with normal control. A statistically significant (P < 0.05) decrease was seen between diabetic control group and other treatment.
Figure 6: Bar chart representation of glucose tolerance assessment in minutes (30, 60, 90, 120 and 150. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

Click here to view


[Figure 7] shows the levels of creatinine expression in normal control and treatment groups. The diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with normal control, there were notable decreases without statistically (P > 0.05) significant difference. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there was a statistically significant (P < 0.05) decrease.
Figure 7: Bar chart representation of creatinine expression levels. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

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[Figure 8] shows the levels of serum corticosterone expression in normal control and treatment groups. Diabetic control revealed a statistically (P < 0.05) significant increase when compared with normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with the normal control showed a notable decrease though there was no statistically (P > 0.05) significant difference. However, comparing groups D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control showed a statistically (P < 0.05) significant decrease.
Figure 8: Bar chart representation of serum corticosterone expression levels. # (statistically significant when compared with normal control group); * (statistically significant when compared with diabetic control group)

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[Figure 9] shows the changes in body weight of the Wistar rats in week 1, the diabetic control revealed a statistically (P < 0.05) significant decrease when compared with normal control. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control showed a statistically (P < 0.05) significant increase and similar findings were observed in week 2.
Figure 9: Bar chart representation showing the body weight changes in weeks. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

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[Figure 10] shows the levels of urea expression in the normal control and treatment groups. Across treatment groups, the diabetic control revealed a significant increase with no statistically (P > 0.05) significant difference when compared with normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with normal control, there were notable decreases with no statistically (P > 0.05) significant difference. However, a statistically (P < 0.05) significant decrease was found between diabetic control group and other treatment groups except D + Pio (10 mg/kg), which showed a significant reduction.
Figure 10: Bar chart representation of showing the levels of urea expression. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

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[Figure 11] shows the levels of pancreas nitrite expression in normal control and treatment groups. The diabetic control revealed a statistically (P < 0.05) significant increase when compared with the normal control. A significant decrease was observed between diabetic control group and other treatment groups with the exception of D + Pio (10 mg/kg), which showed a statistically significant decrease.
Figure 11: Bar chart representation of pancreas nitrite levels. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

Click here to view


[Figure 12] shows the levels of Pancreas MDA expression in normal control and treatment groups. The diabetic control revealed a statistically (P < 0.05) significant increase when compared with the normal control. Comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg) treated groups with normal control, there were significant (P > 0.05) decrease. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there was a statistically (P < 0.05) significant decrease.
Figure 12: Bar chart representation of pancreas MDA expression Levels. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group, MDA: Malondialdehyde

Click here to view


[Figure 13] shows the levels of Pancreas GSH expression in the normal control and treatment groups. Across treatment groups, the diabetic control revealed a statistically significant (P < 0.05) decrease when compared with the normal control. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, there was a statistically significant increase (P < 0.05).
Figure 13: #P < 0.05 Statistically Significant when compared with normal control group); *P < 0.05 Statistically Significant when compared with Diabetic Control group, #: Bar chart representation of Glutathione (GSH) levels

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[Figure 14] shows the assessment result for serum insulin level in normal control and treatment groups. The diabetic control revealed a statistically (P < 0.05) significant decrease when compared with normal control. However, comparing D + MEDd (400 mg/kg), D + MEDd (800 mg/kg), and D + Pio (10 mg/kg)-treated groups with diabetic control, showed a statistically (P < 0.05) significant increase.
Figure 14: Bar chart representation of serum insulin level. #P < 0.05 statistically significant when compared with normal control group); *P < 0.05 statistically significant when compared with diabetic control group

Click here to view



  Discussion Top


Diabetes has been shown to be a global problem that is associated with a lot disorders, affecting several organs of the body of which the kidney is one of such organs which could result from the generation of excessive reactive species such as reactive oxygen and nitrogen species which serves as the foundation to a lot of ailments. Phytochemicals have been shown diabetes and associated disorders in rat models.[12] Results from our study is line with reports from previous studies that Dd has the potency to ameliorate diabetes and associated disorders.[13] Results from this study revealed that treatment with Dd extract has the potency to ameliorate sustained hyperglycemia with associated disorders which could be as a result of phytoconstituent that are contained in the plant.[14] This is in line with reports from other research using plant extracts in the treatment of diabetes and associated disorders in laboratory animals.[15] Following treatment with MEDd on the treatment groups significantly decrease oxidative stress marker induced by STZ on the diabetic Wistar rats. This was also seen in the oral glucose tolerance test on the last day of the experiment with a pretreatment of glucose load and results. MEDd extract was able to decrease the levels of blood glucose in diabetic rats compared to the diabetic nontreated rats which experienced increased blood glucose levels throughout the study which is the major aim of all anti-diabetic study as hyperglycemia is involved in the generations of free radicals that is attributed with diabetes induced disorder.[16]

The mechanism by which STZ induces diabetes is by inhibiting the production of insulin by the pancreatic cells unavoidably needed for the metabolism of glucose to be stored in the liver.[17] This was evident in this study in the negative control group which experienced reduced insulin levels and this was ameliorated in the treated groups as increased levels of insulin was observed. This result is in line reports from previous studies on MEDd where it reduces diabetic levels in Wistar rats that is associated proper utilization of insulin.[13] Sustained hyperglycemia is attributed with complications on several organs of the human system such as the macro- and micro-vascular system, lots of medicinal plants have been able to combat diabetes and its associated complications.[14] Following this MEDd could be used to assist diabetics to ameliorate hyperglycemia.

Oxidative damage experienced in diabetes results from excessive generation reactive species caused by sustained hyperglycemia which leads to oxidative stress that result in the deterioration of tissues and organs that starts from the cells, the levels of oxidation in favors of reactive species deteriorates antioxidant defense mechanism and is also involved in the several complications associated with diabetes.[18]

Elevated levels of blood glucose levels in Wistar rats due to diabetic induction using STZ can also induce excessive production of reactive species in organs such as the kidney and pancreas leading to oxidative damage of such organs resulting the malfunctioning which results from the destruction of the antioxidant defense mechanism system.[19] The elevated levels of nitrate and MDA in organs such as the kidney and pancreas in diabetic Wistar rats induced with STZ was significantly reduced in the treated groups compared to the diabetic untreated group showing the ameliorative capacity of MEDd in this study. Furthermore, in this present study, the levels of the antioxidant defense marker GSH reductase were significantly decreased in the kidney and in the pancreas in the treated groups compared to the negative control group which showed significantly high levels of GSH throughout the period of the study. Furthermore, the effect of the ameliorated levels of GSH in the treated groups was seen in the decreased levels of nitrite and MDA levels in the pancreas and Kidney. This revealed the plant extract possess the capacity to scavenge free radicals that increased its antioxidant potency which is in line with previous reports on MEDd.[13]

MEDd reverses the damage done by STZ-induced diabetes on Wistar rat's kidney biomarkers in the treated groups. The statistically significant level of kidney damage observed in the untreated diabetic group reveals the elevated levels of urea and creatinine activity which otherwise was reduced in the treated groups. One of the most associated disorder of diabetes is nephropathy that results from free radical generation altering the functionality of the nephron.[20] In addition, the protective capacity of the plant extract on the kidney which is observed in its reduced markers in the present study could be attributed to antioxidant capacity to reduce the levels of lipid peroxidation in the kidney and in the pancreas and its ability to significantly increased the levels of antioxidant markers such as GSH reductase after treatment with methanol extract of MEDd which effect was also observed in the reduced weight of kidney and liver in the treated groups compared to the increased kidney and liver weight in the diabetic untreated group that is attributed to diabetes.[21] Moreover, the ability of methanol leaf extract of MEDd enhance the antioxidant defense mechanism of the treated groups revealed its therapeutic potency in ameliorating diabetes and reducing kidney damage observed in diabetes.


  Conclusion Top


Conclusively, the present study has shown that the medicinal plant MEDd possess hypoglycemic capacity, antioxidant, and nephron-protective capacity in STZ-induced diabetes that resulted from the phytoconstituent found in the plant MEDd that is attributed to it potencies.

Acknowledgments

This research did not receive any specific funding.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]



 

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