• Users Online: 35
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 9  |  Issue : 1  |  Page : 25-30

Ethanolic leaf extract of Ipomoea aquatica Forsk abrogates cisplatin-induced hepatotoxicity in albino rats


1 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Niger Delta University, Bayelsa State, Nigeria
2 Department of Pharmacology, Faculty of Basic Medical Sciences, Niger Delta University, Bayelsa State, Nigeria

Date of Submission27-May-2019
Date of Acceptance09-Feb-2020
Date of Web Publication26-Jun-2020

Correspondence Address:
Dr. Elias Adikwu
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Niger Delta University, Bayelsa State.
Nigeria
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrptps.JRPTPS_53_19

Rights and Permissions
  Abstract 

Context: Hepatotoxicity is a therapeutic predicament that affects the clinical use of cisplatin (CPT). Ipomoea aquatica is traditionally used for the treatment of some diseases. This study examined the protective effect of the ethanolic leaf extract of Ipomoea aquatica (EEIA) against CPT-induced hepatotoxicity in albino rats. Materials and Methods: Fifty-four adult male albino rats randomized into nine groups (six rats in each group) were treated orally with EEIA (100, 200, and 400 mg/kg) daily for 7 days and CPT (6 mg/kg) intraperitoneally on day 5 and 7, respectively. On day 8, the rats were anesthetized; blood samples were collected and evaluated for plasma liver function markers. Liver samples were harvested and evaluated for biochemical parameters and histology. Statistical Analysis: Data are presented as mean ± standard error of the mean (SEM). Statistical analysis was performed using one-way analysis of variance (ANOVA) and Tukey’s test. Results: CPT-induced hepatotoxicity was characterized by significant (P < 0.001) elevations in liver and plasma levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, total bilirubin, and conjugated bilirubin when compared to control. The alterations in liver redox status of CPT-treated rats were marked by significant (P < 0.001) decreases in superoxide dismutase, catalase, glutathione, and glutathione peroxidase levels with significant (P < 0.001) increases in malondialdehyde levels when compared to control. The liver of CPT-treated rat was characterized by hepatocyte necrosis. The hepatotoxic effect of CPT was significantly abrogated in a dose-dependent fashion in rats pretreated with EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) when compared to CPT-treated rats. Conclusion: EEIA has potential as treatment for CPT-induced hepatotoxicity.

Keywords: Cisplatin, Ipomoea aquatic, liver, prevention, rat, toxicity


How to cite this article:
Adikwu E, Bokolo B, Kemelayefa J. Ethanolic leaf extract of Ipomoea aquatica Forsk abrogates cisplatin-induced hepatotoxicity in albino rats. J Rep Pharma Sci 2020;9:25-30

How to cite this URL:
Adikwu E, Bokolo B, Kemelayefa J. Ethanolic leaf extract of Ipomoea aquatica Forsk abrogates cisplatin-induced hepatotoxicity in albino rats. J Rep Pharma Sci [serial online] 2020 [cited 2020 Dec 5];9:25-30. Available from: https://www.jrpsjournal.com/text.asp?2020/9/1/25/287589


  Introduction Top


The rapid demise of cancer cells on exposure to chemotherapy has successful reduced cancer-associated mortality.[1] Cisplatin (CPT) is one of the most clinically used drugs for cancer chemotherapy. It has shown good therapeutic outcome against many solid organ malignancies such as brain, neck, testicular, ovarian, and pulmonary cancers.[2] Its mode of action has been linked to its ability to structurally impair purine bases on deoxyribonucleic acid (DNA). This interferes with DNA repair mechanisms, causing DNA damage, and subsequently inducing apoptosis in cancer cells.[3] However, its significant anticancer activity is often affected by numerous toxicities including hepatotoxicity.[4],[5] Hepatotoxicity associated with CPT could be predicated on it biotransformation by the liver. Studies have shown that at higher doses; it can be rapidly absorbed and stored by liver hepatocytes leading to hepatocytes perturbation and dysfunction.[6] Clinically, hepatic perturbations caused by CPT are often characterized by hepatocyte necrosis, steatosis central vein congestion, sinusoidal dilatation, and cell apoptosis.[7],[8] The precise mechanism by which CPT causes hepatotoxicity is not clear, but multiple studies have speculated hepatic oxidative stress (OS) through the generation of free radicals.[9] Also, alterations in hepatic redox status through CPT-glutathione (GSH) adduct formation causing decreases in liver antioxidants have been speculated.[10]

It is estimated that 80% of the world population presently use medicinal plants for the treatment of some diseases. Medicinal plants are important sources of new chemical substances with potential therapeutic effects.[11]Ipomoea aquatica (IPA) is a medicinal plant that belongs to the Convolvulaceae family. It grows in the forest and is also cultivated throughout South East Asia. It is generally consumed as vegetable in different regions of the world. Due to its rapid growth, it is common in rice paddies, fish ponds, and drainage canals.[12] IPA is an effective natural herb used traditionally for the treatment of some ailments[13] including liver disease.[14],[15] Its traditional use can be supported by some pharmacologic activities reported in in-vivo and in-vitro studies.[16] Furthermore, studies have reported the presence of essential and active phytochemicals in IPA which can also attest to its traditional use for the treatments of some ailments.[17] This study explore whether the ethanolic leaf extract of Ipomoea aquatica (EEIA) contains essential phytochemicals that can abrogate CPT-induced hepatotoxicity in a rat model.


  Materials and Methods Top


Drug and plant material

CPT injection used for this study was manufactured by Sun Pharmaceutical, Industries Ltd, Mumbai, India. Fresh leaves of IPA were obtained from Niger Delta University, Nigeria. The leaves were washed thoroughly in water and the surface water was removed by air drying. The leaves were subsequently dried in a hot air oven at 48°C for 36hr and powdered with the aid of a mechanical grinder. For the preparation of ethanolic extract, 350 g of IPA powder was added to 1000 mL of ethanol and macerated for 24h and filtered. The extract was filtered through Whatman No. 1 paper and evaporated under reduced pressure using a rotary evaporator to a dry extract. The extract was analyzed for carbohydrate, protein, tannins, saponins, steroids, flavonoids, terpenoids, alkaloids, and glycosides according to Harborne[18] and Trease and Evans.[19]

Ethical issues

This study was approved by the Research Ethics Committee of the Department of Pharmacology and Toxicology, Faculty of Pharmacy, Niger Delta University, Bayelsa State, Nigeria. The rats were handled according to the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Science.

Experimental protocol and biochemical analyses

Fifty-four adult male albino rats (200–220 g) sourced from the animal breeding facility of the Faculty of Pharmacy, Niger Delta University, Bayelsa State, Nigeria were kept in an environment controlled at 23°C ± 2°C with a 12h light/dark periods. The rats had access to standard rodent chow and water ad libitum and were allowed for 1 week to acclimatize to laboratory conditions prior to the experiment. Group A (solvent control) (n = 6) and Group B (placebo control) (n = 6) were orally treated with normal saline (0.2 mL) and corn oil (0.2 mL) daily for 7 days, respectively. Groups C–E (n = 6/group) were orally treated with EEIA (100, 200, and 400 mg/kg)[20] daily for 7 days, respectively. Group F (n = 6) was treated once with CPT (6 mg/kg) intraperitoneally (i.p.)[21] on day 5 and 7. Groups G–I (n = 6/group) were pretreated orally with EEIA (100, 200, and 400 mg/kg) daily for 7 days, respectively, whereas CPT (6 mg/kg) was administered i.p. on day 5 and 7. After the completion of treatment, the albino rats were sacrificed under inhalational diethyl ether. Blood samples were collected, centrifuged (3000g for 15 min), and plasma samples were separated for biochemical evaluations. Liver samples were excised, rinsed in cold normal saline, and homogenized in 0.1 M Tris-HCl solution buffered (pH 7.4). The homogenates were centrifuged at 1500 g for 30 min and the supernatants were collected and assessed for biochemical indices. Plasma and liver alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), lactate dehydrogenase (LDH), conjugated bilirubin (CB), and total bilirubin (TB) were evaluated using commercial laboratory test kits (Randox Laboratories, Crumlin, UK). Liver total protein was analyzed according to Gornall et al.[22] whereas malondialdehyde (MDA) was analyzed according to Buege and Aust.[23] Reduced glutathione (GSH) was measured as reported by Sedlak and Lindsay.[24] The method of Sun and Zigman[25] was used for the evaluation of superoxide dismutase (SOD), whereas the method of Aebi[26] was used to assay catalase (CAT). Glutathione peroxidase (GPx) was measured as described by Rotruck et al.[27]

Histological evaluation

Liver sections were taken immediately, and fixed in 10% buffered neutral formalin for 24hr. Liver samples were dehydration in increasing concentrations of ethyl alcohol, and embedded in paraffin blocks. The paraffin blocks were sectioned (5–7 µm thick) and stained with hematoxylin and eosin. The sections were examined for the histological changes with the aid of a light microscope.

Statistical analysis

Data are presented as mean ± standard error of the mean (SEM). Data were analyzed using Graph Pad Prism (Version 5.0, Graph Pad Software Inc., La Jolla, California, USA). One-way analysis of variance (ANOVA) was used for comparison among means followed by Tukey’s post hoc tests. Significance was set at P < 0.05, 0.01, and 0.001.


  Results Top


Phytochemical analyses and serum liver function parameters

The evaluation of EEIA shows the presence of flavonoids, glycosides, carbohydrate, alkaloids tannins, saponins, and protein. The plasma levels of AST, ALT, ALP, LDH, GGT, CB and TB were normal (p>0.05) in rats treated with EEIA when compared to control [Table 1]. On the other hand, treatment with CPT significantly increased (P < 0.001) plasma AST (258.6%), ALT (347.8%), ALP (289.5%) LDH (388.0%), GGT (462.3%), CB (213.6%), and TB (346.3%) levels when compared to control [Table 1]. On the contrary, the plasma levels of AST, ALT, ALP, LDH, GGT, CB, and TB were significantly decreased in a dose-dependent fashion in EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) pretreated rats when compared to CPT-treated rats [Table 1].
Table 1: Effect of Ipomoea aquatica leaf extract on liver function parameters of cisplatin-treated rats

Click here to view


Effects on liver tissue biochemical indices

Treatment with EEIA did not produce significant (p>0.05) effects on liver AST, ALT, ALP, LDH, and GGT levels when compared to control [Table 2]. On the other hand, the liver levels of AST, ALT, ALP, LDH, and GGT were significantly (P < 0.001) increased in CPT-treated rats when compared to control [Table 2]. The increases observed in the aforementioned parameters represent 251.0%, 294.7%, 372.3%, 482.8%, and 256.9%, respectively. However, the liver levels of AST, ALT, ALP, LDH, and GGT were significantly decreased in a dose-dependent fashion in rats pretreated with EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) when compared to CPT-treated rats [Table 2].
Table 2: Effect of Ipomoea aquatica leaf extract on liver tissue biochemical indices of cisplatin-treated rats

Click here to view


Effects on liver oxidative stress markers and histology

Treatment with EEIA had no significant (p>0.05) effects on liver CAT, SOD, GSH, GPx and MDA levels when compared to control [Table 3]. However, treatment with CPT produced significant (P < 0.001) decreases in liver CAT, SOD, GSH, and GPx levels with significant (P < 0.001) increase in MDA level when compared to control [Table 3]. On the contrary, MDA levels were significantly decreased whereas CAT, SOD, GSH, and GPx levels were significantly increased in a dose-dependent fashion in rats pretreated with EEIA 100 mg/kg (P < 0.05), 200 mg/kg (P < 0.01), and 400 mg/kg (P < 0.001) when compared to CPT-treated rats [Table 3]. The liver of the control rats showed normal hepatocytes [Figure 1]A. Also, the liver of rats treated with EEA (100, 200, and 400 mg/kg) showed normal hepatocytes, respectively [Figure 1]B–D. However, the liver of rats treated with CPT (6 mg/kg) showed hepatocyte necrosis [Figure 1]E. On the contrary, the liver of rats pretreated with EEIA (100, 200, and 400 mg/kg) showed normal hepatocytes, respectively [Figure 1]F–H.
Table 3: Effect of Ipomoea aquatica leaf extract on liver oxidative stress markers of cisplatin-treated rats

Click here to view
,
Figure 1: (A) Liver of control rat showing normal hepatocytes. (B–D) Liver of rat treated with ethanolic leaf extract of Ipomoea aquatica (100, 200, and 400 mg/kg) showing normal hepatocytes. (E) Liver of rat treated with 6 mg/kg of cisplatin showing hepatocyte necrosis. (F–H) Liver of rats pretreated with ethanolic leaf extract of Ipomoea aquatica (100, 200, and 400 mg/kg) prior to the administration of cisplatin ( 6 mg/kg) showing normal hepatocytes (Hand E X100)

Click here to view



  Discussion Top


This study shows the presence of flavonoids, glycosides, carbohydrate, alkaloids tannins, saponins, and protein in EEIA. This finding is consistent with previous report.[28] The liver contains AST, ALT, ALP, GGT, and LDH in higher concentrations than the serum. Injury to the liver can lead to the leakage of the aforementioned parameters into the serum causing increased serum concentrations.[29] This study observed the leaching of AST, ALT, ALP, GGT, LDH, CB, and TB into systemic circulation confirmed by high plasma levels in CPT-treated rats. This observation is in agreement with previous findings.[30] The observed high levels of AST, ALT, ALP, GGT, LDH, CB, and TB in systemic circulation are clear evidence of the destruction of hepatocyte membrane in CPT-treated rats.[20] However, the functionality of hepatocyte membrane was restored in EEIA-pretreated rats in a dose-dependent fashion as shown by low plasma levels of the aforementioned parameters. OS is a condition that occurs when the steady-state balance of prooxidants to antioxidants is shifted in the direction of the former, causing damage to lipids, proteins, and DNA. Antioxidants including SOD, CAT, GSH and GPx protect biomolecules from OS-induced damage caused by prooxidants such as free radicals. Substantial evidence has shown that excess OS can decrease antioxidant activities.[31] This study observed decreases in SOD, CAT, GSH, and GPx activities in the liver of CPT-treated rats. This observation has been previously reported.[32] This observation shows that OS is a biochemical process in CPT-induced hepatotoxicity. However, upregulations in the activities of SOD, CAT, GSH, and GPx in a dose-dependent fashion were observed in the liver of EEIA-pretreated rats. Lipid peroxidation (LPO) is a biochemical process that leads to the destruction of polyunsaturated fatty acids (PUFA) in cells, thereby impairing their functions and structures. MDA is one of the most readily assayed end products of both enzymatic and nonenzymatic LPO reactions. High tissue level of MDA is used vividly to establish the oxidative destruction of PUFA.[33] This study observed the destruction of PUFA marked by high levels of MDA in the liver of CPT-treated rats. This observation is in agreement with previous report.[34] However, there were evident decreases in the levels of MDA in a dose-dependent fashion in the liver of EEIA-pretreated rats. This observation is an evidence of the inhibitory effect of EEIA on CPT-induced destruction of hepatic PUFA. Furthermore, the liver section of CPT-treated rats showed hepatocyte necrosis. This observation is in agreement with previous studies.[35] However, the observed necrosis in the liver of CPT-treated rats was abrogated in EEIA-pretreated rats. Despite the fact that the mechanism of CPT-induced hepatotoxicity is not fully understood, some studies have speculated hepatic OS through the generation of free radicals.[36] Free radicals can damage biological molecules such as lipids, proteins, and DNA and eventually stimulate cell apoptosis.[37] Also, functional and structural mitochondrial injury and the production of pro-inflammatory mediators have been speculated in CPT-induced hepatotoxicity.[38] In this study, the abrogation of CPT-induced hepatotoxicity by EEIA could be attributed to its phytochemical constituents. EEIA contains flavonoids, tannins, and other phytochemical constituents that have antioxidant activities.[39],[40] Flavonoids are antioxidants that scavenge and chelate free radicals. Also, tannins act as free radical terminators and are involved in the retardation of oxidative degradation of lipids.[41] The presence of these phytochemical constituents in EEIA might have inhibited, scavenged, or neutralized CPT-induced free radical production in the liver, thereby preventing hepatotoxicity.


  Conclusion Top


Ipomoea aquatica Forsk contains essential phytochemical(s) that may be used as treatment for hepatotoxicity caused by CPT.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
DeVita VT Jr, Chu E. A history of cancer chemotherapy. Cancer Res 2008;68:8643-53.  Back to cited text no. 1
    
2.
Jordan P, Carmo-Fonseca M. Molecular mechanisms involved in cisplatin cytotoxicity. Cell Mol Life Sci 2000;57:1229-35.  Back to cited text no. 2
    
3.
Díaz R, Jordá MV, Reynes G, Aparicio J, Segura A, Amador R, et al. Neoadjuvant cisplatin and etoposide with or without tamoxifen, prior to radiotherapy in high-grade gliomas: A single-center experience. Anti Can Drugs 2005;16:323-9.  Back to cited text no. 3
    
4.
Işeri S, Ercan F, Gedik N, Yüksel M, Alican I. Simvastatin attenuates cisplatin-induced kidney and liver damage in rats. Toxicol 2007;230:256-64.  Back to cited text no. 4
    
5.
Zicca A, Cafaggi S, Mariggiò MA, Vannozzi MO, Ottone M, Bocchini V, et al. Reduction of cisplatin hepatotoxicity by procainamide hydrochloride in rats. Eur J Pharmacol 2002;442:265-72.  Back to cited text no. 5
    
6.
Hesketh MA, Twaddell T, Finn AA. Possible role for cisplatin (DDP) in the transient hepatic enzyme elevation noted after ondansetron administration. Proc Am Assoc Clin Oncol 1990; 9:323.  Back to cited text no. 6
    
7.
Ciftci O, Onat E, Cetin A. The beneficial effects of fish oil following cisplatin-induced oxidative and histological damage in liver of rats. Iran J Pharm Res 2017;16:1424-31.  Back to cited text no. 7
    
8.
Attyah AM, Ismail SH. Protective effect of ginger extract against cisplatin-induced hepatotoxicity and cardiotoxicity in rats. Iraqi J Pharm Sci 2012;21:27-33.  Back to cited text no. 8
    
9.
Masuda H, Tanaka T, Takahama U. Cisplatin generates superoxide anion by interaction with Dna in a cell-free system. Biochem Biophys Res Commun 1994;203:1175-80.  Back to cited text no. 9
    
10.
Kharbangar A, Khynriam D, Prasad SB. Effect of cisplatin on mitochondrial protein, glutathione, and succinate dehydrogenase in Dalton lymphoma-bearing mice. Cell Biol Toxicol 2000;16:363-73.  Back to cited text no. 10
    
11.
Ehigiator EB, Adikwu E. Ethanolic extract of chrysophyllumalbidumstem bark prevents alloxan-induced diabetes not. Sci Biol 2019;11: 325-31.  Back to cited text no. 11
    
12.
Patnaik S. Autoecology of Ipomoea aquatica Forsk. J Inland Fish Soc India 1976;8:77-82.  Back to cited text no. 12
    
13.
Facciola S. Cornucopia: A Source Book of Edible Plants. 2nd ed. TX, USA:Kampong Publications;1990.  Back to cited text no. 13
    
14.
Badruzzaman SM, Husain W. Some aquatic and marshy land medicinal plants from Hardoi district of Uttar Pradesh. Fitoter 1992;63:245-7.  Back to cited text no. 14
    
15.
Dewanjee S, Dua TK, Khanra R, Das S, Barma S, Joardar S, et al. Water spinach, Ipomoea aquatica (convolvulaceae), ameliorates lead toxicity by inhibiting oxidative stress and apoptosis. PLoS One 2015;10:e0139831.  Back to cited text no. 15
    
16.
Malakar C, Choudhury PN. Pharmacological potentiality and medicinal uses of Ipomoea aquatica Forsk: A review. Asian J Pharm Clin Res 2015;8:60-3.  Back to cited text no. 16
    
17.
Umar KJ, Muhammad MJ, Sani NA, Muhammad S, Umar MT. Comparative study of antioxidant activities of the leaves and stem of Ipomoea aquatica Forsk (water spinach). Niger J Basic Appl Sci 2015;23:81-4.  Back to cited text no. 17
    
18.
Harborne JB. Phytochemical Methods: A Guide to Modern Techniques of Plant Analysis. 3rd ed. London, UK:Chapman and Hall;1973.  Back to cited text no. 18
    
19.
Trease GE, Evans WC. Textbook of Pharmacognosy. 14th ed. London, UK:Harcourt, Brace and Company;2002.  Back to cited text no. 19
    
20.
Alkiyumi SS, Abdullah MA, Alrashdi AS, Salama SM, Abdelwahab SI, Hadi AH. Ipomoea aquatica extract shows protective action against thioacetamide-induced hepatotoxicity. Molecules 2012;17:6146-55.  Back to cited text no. 20
    
21.
Mika D, Guruvayoorappan C. The effect of Thespesia populnea on cisplatin induced nephrotoxicity. J Cancer Res Ther 2013;9:50-3.  Back to cited text no. 21
    
22.
Gornall AG, Bardawill CJ, David MM. Determination of serum proteins by means of the biuret reaction. J Biol Chem 1949;177:751-66.  Back to cited text no. 22
    
23.
Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzymol 1978;52:302-10.  Back to cited text no. 23
    
24.
Sedlak J, Lindsay RH. Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman’s reagent. Anal Biochem 1968;25:192-205.  Back to cited text no. 24
    
25.
Sun M, Zigman S. An improved spectrophotometric assay for superoxide dismutase based on epinephrine autoxidation. Anal Biochem 1978;90:81-9.  Back to cited text no. 25
    
26.
Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121-6.  Back to cited text no. 26
    
27.
Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra WG. Selenium: Biochemical role as a component of glutathione peroxidase. Science 1973;179:588-90.  Back to cited text no. 27
    
28.
Bokolo B, Adikwu E. Ethanolic leaf extract of Ipomoea aquatica Forsk abrogates cisplatin-induced kidney damage in albino rats. J Nephropharm 2019;8:1-7  Back to cited text no. 28
    
29.
Adikwu E, Bokolo B. Effect of cimetidine on cyclophosphamide-induced liver toxicity in albino rats. Asian J Med Sci 2018;9: 51-65.  Back to cited text no. 29
    
30.
Karadeniz A, Simsek N, Karakus E, Yildirim S, Kara A, Can I, et al. Royal jelly modulates oxidative stress and apoptosis in liver and kidneys of rats treated with cisplatin. Oxid Med Cell Longevity 2011;2011:981793.  Back to cited text no. 30
    
31.
Halliwell B. Biochemistry of oxidative stress. Biochem Soc Trans 2007;35:1147-50.  Back to cited text no. 31
    
32.
Yüce A, Ateşşahin A, Ceribaşi AO, Aksakal M. Ellagic acid prevents cisplatin-induced oxidative stress in liver and heart tissue of rats. Basic Clin Pharmacol Toxicol 2007;101:345-9.  Back to cited text no. 32
    
33.
Draper HH, Hadley M. Malondialdehyde determination as index of lipid peroxidation. Methods Enzymol 1990;186:421-31.  Back to cited text no. 33
    
34.
An Y, Xin H, Yan W, Zhou XX. Amelioration of cisplatin-induced nephrotoxicity by pravastatin in mice. Exp Toxicol Pathol 2011;63: 215-9.  Back to cited text no. 34
    
35.
Palipoch S, Punsawad C. Biochemical and histological study of rat liver and kidney injury induced by cisplatin. J Toxicol Pathol 2013;26: 293-9.  Back to cited text no. 35
    
36.
Bentli R, Parlakpinar H, Polat A, Samdanci E, Sarihan ME, Sagir M. Molsidomin prevents cisplatin-induced hepatotoxicity. Arch Med Res 2013;44:521-8.  Back to cited text no. 36
    
37.
Palipoch S, Punsawad C, Koomhin P, Suwannalert P. Hepatoprotective effect of curcumin and alpha-tocopherol against cisplatin-induced oxidative stress. Bmc Complement Altern Med 2014;14:111.  Back to cited text no. 37
    
38.
Ezz-Din D, Gabry MS, Farrag AR, Abdel Moneim AE. Physiological and histological impact of Azadirachta indica (neem) leaves extract in a rat model of cisplatin-induced hepato and nephrotoxicity. J Med Plants Res 2011;5:5499-06.  Back to cited text no. 38
    
39.
Huang DJ, Chen HJ, Lin CD, Lin YH. Antioxidant and antiproliferative activities of water spinach (Ipomoea aquatica Forsk) constituents. Bot Bull Acad Sinica 2005;46:99-106.  Back to cited text no. 39
    
40.
Khatun CS, Islam A, Azad AK, Ali A, Hassan F, Wahidunnobi M. Antibacterial, antidiabetic and lipid lowering effects of ethanolic extract of ipomoea aquatica Bangladesh J Microbiol 2012;29:50-4.  Back to cited text no. 40
    
41.
Pourmorad F, Hosseinimehr SJ, Shahabimajd N. Antioxidant activity, phenol and flaconoids content of some selected Iranian plants. Afr J Biotech 2006;5:1142-5.  Back to cited text no. 41
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and Me...
Results
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed732    
    Printed51    
    Emailed0    
    PDF Downloaded126    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]