• Users Online: 135
  • Print this page
  • Email this page


 
 
Table of Contents
ORIGINAL ARTICLE
Year : 2021  |  Volume : 9  |  Issue : 4  |  Page : 259-264

Evaluation of hepatoprotective activity of leaf decoction of Ficus semicordata Buch.-Ham. ex Sm. in Charles Foster albino rats


1 State Ayurvedic Dispensary, Dubeychapra, Ballia, Uttar Pradesh, India
2 Department of Dravyaguna, Institute for Teaching and Research in Ayurveda, Jamnagar, Gujarat, India
3 Department of Pharmacology Laboratory, Institute for Teaching and Research in Ayurveda, Jamnagar, Gujarat, India

Date of Submission03-Jun-2021
Date of Decision09-Sep-2021
Date of Acceptance24-Sep-2021
Date of Web Publication29-Dec-2021

Correspondence Address:
Prof. Shashi Gupta
State Ayurvedic Dispensary, Dubeychapra, Ballia 277403, Uttar Pradesh.
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jism.jism_53_21

Rights and Permissions
  Abstract 

Background: Bhuidumri, distinctive of the folklore floras of Odisha, is recognized as Ficus semicordata Buch.-Ham. ex Sm., family Moraceae. The leaves of Bhuidumri are recounted for their traditional usage and they are used to treat jaundice, stomach ailments, wound, indigestion, liver ailment, and skin diseases. The present research article aims at exploring the hepatoprotective activity of leaf decoction of F. semicordata in Charles Foster albino rats. Materials and Methods: The dried leaves of F. semicordata were prepared into powder, and the decoction (kwatha) form was used in accordance with the Ayurvedic Pharmacopeia of India. The hepatoprotective activity of a trial drug (4.5 mL/kg, po) was assessed against thioacetamide-persuaded hepatotoxicity in Charles Foster albino rats. Silymarin (100 mg/kg, po) was used as a reference standard drug in a positive control group. Results: Thioacetamide-treated rats revealed a nonsignificant increase in SGPT (665.00 ± 298.96) and SGOT (1196.67 ± 540.38) in comparison with the normal control group. The F. semicordata kwatha-treated group revealed a nonsignificant increase in SGPT (1091.80 ± 558.23) and SGOT (2652.00 ± 944.83) in comparison with the thioacetamide control group. Sylimarin revealed a nonsignificant decrease in SGPT (110.80 ± 20.62) and SGOT (425.60 ± 157.74) in comparison with the thioacetamide control group. Microscopic examination of liver sections from normal control rats exhibited normal cytoarchitecture; thioacetamide-administered rats and F. semicordata kwatha-treated group with thioacetamide showed severe centrilobular necrosis and polymorphonuclear leukocytes (PMN) infiltration, multifocal Grade [3]. The reference standard group-treated groups showed mild necrosis and PMN infiltration with fatty changes, Grade [1]. Conclusion: F. semicordata leaf kwatha is nonhepatoprotective on thioacetamide-induced liver toxicity in rats at the given dose and dosage form.

Keywords: Bhuidumri, Ficus semicordata, hepatoprotective, silymarin, thioacetamide


How to cite this article:
Gupta S, Acharya R, Nariya MB. Evaluation of hepatoprotective activity of leaf decoction of Ficus semicordata Buch.-Ham. ex Sm. in Charles Foster albino rats. J Indian Sys Medicine 2021;9:259-64

How to cite this URL:
Gupta S, Acharya R, Nariya MB. Evaluation of hepatoprotective activity of leaf decoction of Ficus semicordata Buch.-Ham. ex Sm. in Charles Foster albino rats. J Indian Sys Medicine [serial online] 2021 [cited 2022 Oct 3];9:259-64. Available from: https://www.joinsysmed.com/text.asp?2021/9/4/259/334259




  Introduction Top


Bhuidumri, Ficus semicordata Buch.-Ham. ex Sm., of Moraceae family, is a small or medium-sized evergreen tree, having oblong or semi-sagittate leaves, hispid above, petioles-scabrid, receptacles in pairs or clusters on leaflets, drooping branches, ripens reddish fruits.[1] The leaves of Bhuidumri are known for their traditional practices to treat jaundice,[2] and they are also noted for their antioxidant[3] and hepatoprotective activity.[4] This study explores the unreported, hepatoprotective activity of leaf decoction of F. semicordata in albino rats.


  Materials and Methods Top


Collection of Plants

F. semicordata, distinguished as Bhuidumri, was collected from its natural source Paikmal, Odisha, during November 2017; its leaves were collected and authenticated by a taxonomist and by the Botanical Survey of India (Certificate no. CNH/Tech.II/2018/11).

Animals

Charles Foster albino rats of each sex weighing 200 ± 20 g were used for the trials. The animals were acquired from the Animal house attached to Pharmacology, Institute for Teaching and Research in Ayurveda (Reg. no: 548/GO/ReBi/S/02/CPCSEA), Gujarat Ayurveda University, Jamnagar. The animals were kept in a cage made up of polypropylene with a stainless steel top grill. The dry wheat (post hulled) surplus was used as bedding material and was changed every morning. The selected animals were set aside under acclimatization one week before the experiments. The animals were sustained as per standard husbandry settings in affinities of temperature (22 ± 3ºC), relative humidity (50%–60%), and 12-h light and dark cycles. The animals were harbored with VRK brand rat pellet feed conveyed by Keval Sales, Vadodara. The drinking water was given ad libitum. The investigations were conceded out after obtaining the consent of the Institutional Animal Ethics Committee (IAEC/24/2018/25) in compliance with the guidelines of the CPCSEA, New Delhi.

Drug Derivation

Decoction

Accurately weighed 12.5 g coarse powder of leaves of F. semicordata was taken and 50 mL of water was added (1:4 ratio) and was boiled till it was reduced to one-fourth of the total quantity of added water and then it was filtered.[5]

Drug Schedule

The trial drug and vehicle (water administered) to control was between 08:30 am and 9:30 am. The dose of the drugs was fixed by assuming the human dose to laboratory animals on the basis of the body surface area ratio.[6] The deliberate doses and groups for the dosage form of F. semicordata are as follows in [Table 1].
Table 1: Calculated doses and grouping for the dosage form of Ficus semicordata leaf decoction

Click here to view


The trial drugs and distilled water to particular groups were administered for nine successive days. Silymarin (100 mg/kg, po) was used as a reference standard drug in the positive control group. On the ninth day, after 1 h of drug administration, thioacetamide was inoculated intraperitoneally with a dose of 400 mg/kg body weight of rats except to the normal control group (I).[7] After 24 h, the blood was collected from retro-orbital puncturing by a capillary tube under light ether anesthesia. The animals were fasted overnight before the collection of blood samples. Thereafter, animals were sacrificed and liver was dissected out, cleaned off, and wet weight was noted down. The liver was stored in 10% buffered formalin solution and referred for histopathological studies.

Statistical Analysis

The facts are expressed as mean ± standard error of mean (SEM) for six rats per trial group. The statistics engendered during the study was scrutinized by employing Student t-test for paired and unpaired data, and one-way analysis of variance was tracked by Dunnett’s multiple t-test for unpaired data to define the significant difference between groups at P < 0.05.


  Results Top


Effects on Ponderal Changes

Data related to the outcome of test drugs on the bodyweight of albino rats during thioacetamide-induced hepatotoxicity are represented in [Table 2]. The normal control, thioacetamide, F. semicordata leaf Kwatha, and silymarin-treated rats revealed a significant increase in body weight in comparison with initial body weight.
Table 2: Effect of test drugs on body weight during thioacetamide-induced hepatotoxicity in rats (paired t-test)

Click here to view


Data related to the outcome of test drugs on the relative weight of the liver of albino rats are represented in [Table 3]. Thioacetamide-treated rats do not reveal any effect in the relative weight of the liver in comparison with the normal control group. Test drugs did not mark the relative weight of the liver to a noteworthy extent in comparison with the thioacetamide control group.
Table 3: Effect of test drugs on relative weight of liver during thioacetamide-induced hepatotoxicity in rats

Click here to view


Effect on Serum Biochemical Parameters

Data related to the outcome of test drugs on serum triglyceride and high-density lipoprotein (HDL)-cholesterol levels during thioacetamide-induced hepatotoxicity in rats are represented in [Table 4]. Thioacetamide-treated rats revealed a nonsignificant increase (84.67 ± 12.42) in serum triglyceride and a significant decrease (31.33 ± 2.80) in HDL-cholesterol in comparison with the normal control group. F. semicordata kwatha-treated group revealed a nonsignificant increase (120.60 ± 32.63) in triglyceride and a decrease (28.40 ± 2.34) in HDL-cholesterol in comparison with the thioacetamide control group. Sylimarin revealed a significant decrease (67.17 ± 14.84) in serum triglyceride and a nonsignificant decrease (22.67 ± 1.12) in HDL-cholesterol in comparison with the thioacetamide control group.
Table 4: Effect of test drugs on triglyceride and HDL-cholesterol during thioacetamide-induced hepatotoxicity in rats

Click here to view


Data related to the outcome of test drugs on LDL-cholesterol and blood urea levels during thioacetamide-induced hepatotoxicity in rats are represented in [Table 5]. Thioacetamide-treated rats revealed a significant increase (22.67 ± 3.12) in LDL-cholesterol and a nonsignificant increase (53.33 ± 9.87) in urea in comparison with the normal control group. The F. semicordata kwatha-treated group revealed a nonsignificant increase (25.33 ± 9.33) in LDL-cholesterol and (61.40±16.59) blood urea levels in comparison with the thioacetamide control group. Sylimarin revealed a significant decrease (8.25 ± 4.38) in LDL-cholesterol and a nonsignificant decrease (46.33 ± 13.55) in urea levels in comparison with the thioacetamide control group.
Table 5: Effect of test drug on serum LDL-cholesterol and blood urea during thioacetamide-induced hepatotoxicity in rats

Click here to view


Data related to the outcome of test drugs on alanine aminotransferase (SGPT) and aspartate aminotransferase (SGOT) levels during thioacetamide-induced hepatotoxicity in rats are represented in [Table 6]. Thioacetamide-treated rats revealed a nonsignificant increase in SGPT (665.00 ± 298.96) and SGOT (1196.67 ± 540.38) in comparison with the normal control group. The F. semicordata kwatha-treated group revealed a nonsignificant increase in SGPT (1091.80 ± 558.23) and SGOT (2652.00 ± 944.83) in comparison with the thioacetamide control group. Sylimarin revealed a nonsignificant decrease in SGPT (110.80 ± 20.62) and SGOT (425.60 ± 157.74) in comparison with the thioacetamide control group.
Table 6: Effect of test drug on SGPT and SGOT during thioacetamide-induced hepatotoxicity in rats

Click here to view


Data related to the outcome of test drugs on serum alkaline phosphatase (ALP) and cholesterol levels during thioacetamide-induced hepatotoxicity in rats are represented in [Table 7]. Thioacetamide-treated rats revealed a highly significant increase (206.50 ± 3.32) in ALP and a nonsignificant increase (73.67 ± 5.86) in cholesterol in comparison with the normal control group. The F. semicordata kwatha-treated group revealed a nonsignificant increase (212.60±35.72) in ALP and a nonsignificant decrease (59.40 ± 9.24) in cholesterol in comparison with the thioacetamide control group. Sylimarin revealed a nonsignificant decrease (168.67 ± 21.95) in ALP and a significant decrease (38.00 ± 3.93) in cholesterol in comparison with the thioacetamide control group.
Table 7: Effect of test drug on serum alkaline phosphatase and cholesterol during thioacetamide-induced hepatotoxicity in rats

Click here to view


Effect on Cytoarchitecture of Liver

Microscopic examination of liver sections from normal control rats revealed normal cytoarchitecture. Thioacetamide-administered rats and the F. semicordata kwatha-treated group with thioacetamide revealed severe centrilobular necrosis and polymorphonuclear leukocytes (PMN) infiltration, multifocal grade.[3] Sections of liver from the reference standard group-treated groups revealed mild necrosis and PMN infiltration with fatty changes, Grade [1] [Figure 1]A–H.
Figure 1: A. Normal control group (1×100 magn.). B. Normal control group (1×400 magn.). C. Thioacetamide control group (1×100 magn.). D. Thioacetamide control group (1×400 magn.). E. Ficus semicordata leaf kwatha group (1×100 magn.). F. Ficus semicordata leaf kwatha group (1×400 magn.). G. Standard control group (1×100 magn.). H. Standard control group (1×400 magn.)

Click here to view



  Discussion Top


Thioacetamide extensively metabolized to acetamide and thioacetamide dioxide through a mixed-function oxidase system.[8 The mechanism of thioacetamide toxicity is due to the development of thioacetamide dioxide],[ which is responsible for regulating cell permeability and Ca++ concentration],[ increasing the volume of the cell nucleus],[ and also hindering the activity of mitochondria],[ which is an indication of cell death.[9]

In the thioacetamide control group, a statistically nonsignificant increase in the liver weight was observed. It is suggestive of thioacetamide-induced hepatomegaly and liver tissue damage associated with inflammation and fibrosis. The results are substantiating with adverse changes seen in histopathological studies of the liver.

As an indicator of liver damage caused by thioacetamide, SGOT, SGPT, ALP, and total bilirubin were significantly increased, and total protein was decreased.[10] Elevated serum enzyme levels indicate cell loss and loss of functional integrity of liver cell membranes.[11]

Sylimarin produced a nonsignificant decrease in serum transaminases levels in comparison with the thioacetamide control group. The F. semicordata kwatha-treated group produced a nonsignificant increase in serum transaminases levels in comparison with the thioacetamide control group. Thus, an elevation in the transaminase activity can be considered as an index of thioacetamide-induced hepatic injury and its reversal by reference standards is a sign of expression of hepatoprotection, but it is absent in the case of the F. semicordata kwatha-treated group. This effect correlates well with the histopathological examination.

In the present study, significant elevations in the ALP activity being observed in thioacetamide controls in comparison with normal controls. This elevation may be due to cholestasis in the biliary tract, leading to liver injury and henceforth, it can be measured as one of the biomarkers for the assessment of thioacetamide-induced hepatic injury. This elevation was a nonsignificant increase by test drugs and a nonsignificant decrease by standard drugs, thus showing the effect of reference standard on thioacetamide, but no effects were observed in the case of the F. semicordata kwatha-treated group.

The analysis of serum biochemical parameters confirms that administration of thioacetamide leads to significant adverse changes in liver functions related to serum parameters. These altered serum biochemical parameters were reversed by reference standards, but no effects were observed in the F. semicordata leaf kwatha-treated group in reverting serum biochemical parameters, at the given dose and duration.


  Conclusion Top


F. semicordata leaf kwatha is nonhepatoprotective on thioacetamide-induced liver toxicity in rats at the given dose and dosage forms. Pharmacology studies can be done at different doses and in different dosage forms.

Acknowledgment

The authors would like to acknowledge the Director, Institute for Teaching and Research in Ayurveda, Gujarat, Jamanagar for providing all facilities and Ministry of AYUSH for providing financial assistance for the research work, as a part of PhD research project.

Financial support and sponsorship

Ministry of AYUSH as a part of PhD research work at ITRA, Jamnagar.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Saxena HO, Brahmam M. Flora of Orrisa. Vol. 3, 1st ed. Bhubaneswar: Orissa Forest Development Corporation Ltd.; 1995. p. 1703-22.  Back to cited text no. 1
    
2.
Gupta S, Acharya RN, Harisha CR, Shukla V, Hegde S. Detailed pharmacognostical, phytochemical screening and DNA barcoding of leaves of Ficus semicordata Buch.-Ham. ex Sm. (Bhumi Udumbara): An extrapharmacopoeial drug of Ayurveda. Int J Pharm Res 2020;12:1123-31.  Back to cited text no. 2
    
3.
Gupta S, Acharya R. Antioxidant and nutritional evaluation of Bhu Udumbara (Ficus semicordata Buch.-Ham. ex Sm.) leaves and fruits: An extra pharmacopoeial drug of Ayurveda. Ayu 2019;40:120-6.  Back to cited text no. 3
    
4.
Gupta S, Ranade A, Gayakwad S, Acharya R, Pawar S. Hepatoprotective activity of Ficus semicordata Buch.-Ham.ex Sm. leaves aqueous extract on d-galactosamine induced toxicity in HepG2 cell line. Indian J Nat Prod Resour 2020;11:239-43.  Back to cited text no. 4
    
5.
Anonymous. Ayurvedic Formulary of India, Part 1. Appendices, 2nd revised English edition. New Delhi: GOI, Ministry of Health and Family Welfare, ISM and H; 2003. p. 353.  Back to cited text no. 5
    
6.
Paget GE, Barnes JM. Evaluation of drug activities. In: Lawrence DR, Bacharach AL, editors. Pharmacometricseds.Vol. 1. New York: Academic Press; 1964. p. 161.  Back to cited text no. 6
    
7.
Zargar S. Protective effect of Trigonella foenum-graecum on thioacetamide induced hepatotoxicity in rats. Saudi J Biol Sci 2014;21:139-45.  Back to cited text no. 7
    
8.
Dhingra M, Nain P, Nain J, Mailik M. Hepatotoxicity v/s hepatoprotective agents: A pharmacological review. Int Res J Pharm 2011;2:31-7.  Back to cited text no. 8
    
9.
Ambrose AM, DeEds F, Rather LJ. Further studies on toxicity of thioacetamide in rats. Proc Soc Exp Biol Med 1950;74:132-4.  Back to cited text no. 9
    
10.
Ahmad , Pillai KKA, Najmi AK, Ahmad S, Pal SN, Pal SN. Evaluation of hepatoprotective potential of jigrine post-treatment against thioacetamide induced hepatic damage. J Ethnopharmacol 2002;79:35-41.  Back to cited text no. 10
    
11.
Drotman RB, Lawhorn GT. Serum enzymes as indicators of chemical induced liver damage. Drug Chem Toxicol1978;1:163-71.  Back to cited text no. 11
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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
    Viewed406    
    Printed34    
    Emailed0    
    PDF Downloaded40    
    Comments [Add]    

Recommend this journal