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 Table of Contents  
Year : 2021  |  Volume : 6  |  Issue : 1  |  Page : 12-19

Polygonum persicaria L. alleviated oxidative damage and hepatotoxicity induced by carbon tetrachloride in Wistar rats

1 Department of Zoology, Sri Satya Sai University of Technology and Medical Sciences, Sehore, Madhya Pradesh 466001, India
2 Department of Pharmacy, Rajiv Gandhi Proudyogiki Vishwavidhyalay, Bhopal, Madhya Pradesh 462033, India
3 Department of Botany, Barkatullah University, Bhopal, Madhya Pradesh 462023, India

Date of Submission22-Jul-2021
Date of Acceptance21-Sep-2021
Date of Web Publication14-Dec-2021

Correspondence Address:
Dr. Mohd Shafi Dar
Department of Zoology, Sri Satya Sai University of Technology and Medical Sciences, Sehore, Madhya Pradesh 466001.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jdras.jdras_66_21

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BACKGROUND AND OBJECTIVE: Liver illnesses can be metabolic, poison-induced, or infectious and are the fifth greatest cause of death worldwide. Several traditional medicinal plants have been utilized to treat liver diseases in the past. The goal of this study is to see how effective an aqueous extract of Polygonum persicaria L. roots is in protecting the liver from CCl4 toxicity in adult Wistar rats. MATERIALS AND METHODS: Aqueous extract of P. persicaria L. root sections was tested in CCl4-injured Wistar rats in vitro and in vivo. Animals were randomly assigned to normal control, toxic control, standard control (silymarin 100 mg/kg) groups and P. persicaria L. (200 and 400 mg/kg) treatment groups. Histopathology and serum biochemical markers of liver damage were investigated. The extract was examined for phytochemicals and 1,1-diphenyl-2-picrylhydrazyl (DPPH) in vitro. RESULTS: Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin levels in CCl4-damaged rats were all balanced after oral administration of the aqueous extract at 200 and 400 mg/kg/BW/day. In addition, when compared with silymarin therapy, histology of the liver revealed that P. persicaria L. restored tissue injury. Alkaloids, flavonoids, tannins, sterols, and saponins were found to be present in P. persicaria L. The actions of antioxidants are shown in the DPPH method. CONCLUSION: According to the results of this study, P. persicaria L. can reduce hepatotoxicity and oxidative pressure in vitro and in vivo. The ability of the extract to prevent lipid peroxidation and boost antioxidant enzymatic activity could account for this effect.

Keywords: Antioxidant, CCl4, hepatoprotection, histopathology, Polygonum persicaria L., serum enzymes

How to cite this article:
Dar MS, Tahir A, Tabasum S, Najar RA, Mittal DK. Polygonum persicaria L. alleviated oxidative damage and hepatotoxicity induced by carbon tetrachloride in Wistar rats. J Drug Res Ayurvedic Sci 2021;6:12-9

How to cite this URL:
Dar MS, Tahir A, Tabasum S, Najar RA, Mittal DK. Polygonum persicaria L. alleviated oxidative damage and hepatotoxicity induced by carbon tetrachloride in Wistar rats. J Drug Res Ayurvedic Sci [serial online] 2021 [cited 2022 Dec 7];6:12-9. Available from: http://www.jdrasccras.com/text.asp?2021/6/1/12/332501

  Introduction Top

Liver is an essential metabolic organ for biotransformation and detoxification of endogenous and exogenous dangerous constituents.[1],[2] Despite enormous breakthroughs in contemporary medicine, liver illness remains a worldwide health problem, necessitating the continual quest for new medications. There are a variety of medicinal formulations in Ayurveda which are indicated for the treatment of liver disorders.[3] The fundamental oxidative stress-induced liver injury component includes disruption in oxidation and antioxidant arrangements, resulting in an increase in free radicals and a decrease in antioxidant capability. Oxidative stress may result in hepatic fibrosis, cirrhosis, and even hepatocellular carcinoma.[4] Poisons and medications as well as viral infections (hepatitis A, B, C, D) and Entamoeba histolytica microbial infections cause damage to hepatocytes. In this way, hepatocytes are also harmed.[5],[6] Given the several harmful side effects of synthetic medicines, there is a growing emphasis placed on utilization of systematic research techniques, evaluating the scientific basis for traditional herbal treatments which are claimed to have hepatoprotective efficacy.[7] A single medicine cannot treat all types of serious liver disorders.[8] As a result, an effective medicinal plant formulation, as well as relevant pharmacological investigations and clinical trials, needs to be developed.

Drug-induced liver toxicity is responsible for acute liver failure in approximately half of the cases of hepatic pathologies.[9]

Effective therapeutic agents, especially natural compounds with low toxicity, are in high demand right now. Despite the widespread use of mono- and poly-herbal medicines for liver infections,[10] only a few (such as silymarin) have been licensed for use in liver disease prevention or therapy.[11] In recent years, however, some phyto-anti-hepatotoxin products have been associated with liver injury.[12],[13],[14],[15],[16]

Carbon tetrachloride (CCl4), an assembling substance, is a profoundly harmful hepatotoxic specialist which has been widely utilized in animal models to cause acute and chronic liver damage.[17] CCl4 has no cytotoxic consequences for the liver; however, its metabolites such as CCl3 and OOCCl3 cause hepatotoxicity in hepatic parenchyma cells framed by cytochrome P-450 ward monooxygenases.[18] Despite significant advances in modern pharmacotherapies for the treatment of liver illnesses, these drugs are occasionally ineffective and have unwanted adverse effects, especially when used for a long time.

In recent years, there has been a lot of focus on the role of oxygen-free radicals in a variety of diseases. Dynamic oxygen atoms such as superoxide and hydroxyl radicals have been shown to play a role in the inflammatory process. Because of the incomplete reduction of O2, reactive oxygen species (ROS) are created during expanded metabolic states. ROS are a vital part of life. However, there is increased use of energy and the production of more ROS during persistent or intermittent pressure. When the number of ROS in a population exceeds the body’s ability to destroy them, they begin to damage cells and tissues, and organs in cases of chronic stress. ROS also cause mitochondrial damage, which reduces the ability of cells to maintain energy levels.[19]

Many plant extracts and plant products have been demonstrated to have significant antioxidant activity,[20],[21] which could be a significant therapeutic plant property related to the treatment of a few doomed infections such as liver poisonousness. As a result, natural plants are getting recognized as a valuable means of preventing and/or alleviating specific problems such as atherosclerosis, diabetes, hepatotoxicity, and other issues.[20],[22]

Polygonumpersicaria L. is native to tropical Asia and temperate, including the Caucasus, Siberia, China, Eastern Asia, Western Asia, Middle Asia, Indo-China, Indian Subcontinent, Russian Far East, and Malesia; temperate and tropical Europe, including Middle Europe, Northern Europe, East Europe, South-eastern Europe, and Southwestern Europe, as well as Northern Africa and Australia.[23] The plant grows in wet areas such as riverbanks and swamps,[24] and it is usually dominant in agricultural fields.[25]P. persicaria L., in particular, has a wide range of common medicinal applications. In Europe, the plant has been used as an emetic and a diuretic,[26] as well as to treat gynecological disorders.[27] Dyspepsia, itching scalp, diarrhea, hemorrhoids, and frequent menstrual bleeding are often treated with a decoction of the whole herb, either individually or in combination with other restorative herbs.[28] The leaves and seeds are utilized in people’s medication against malignant growth.[29] A few studies on the therapeutic activities of P. persicaria L. are available to help with the plant’s ethnomedicinal uses, which include cancer prevention, antibacterial, antifungal, antihelminth, antifeedant, cytotoxicity, relaxing, estrogenicity, richness, antiadipogenicity, anticholinesterase, and neuroprotection. However, the bioactive complexes and biotic actions in the diverse extraction solvents have not been examined. Therefore, the current work focussed on assessing the antioxidant and hepatoprotective properties of the P. persicaria L. aqueous extract in carbon tetrachloride (CCl4)-induced hepatotoxicity in rats.

  Materials and Methods Top

Plant material and preparation of extract

P. persicaria L. root sections were collected near the Jhelum River in Lethpora, Pampore, Kashmir. The specimen was identified at the Centre for Biodiversity and Taxonomy, Department of Botany, University of Kashmir, using a voucher specimen Herbarium no. 2925 (KASH). The dried roots were macerated in distilled water for 7 days (1:10 drug: solvent ratio). After purifying the sample with cotton, it was collected in a rotatory evaporator at reduced pressure and a maximum temperature of 40°C to obtain a soft extract of P. persicaria.


Silymarin was provided as a free sample by Pinnacle Biomedical Research Institute (PBRI), Bhopal, India. Trichloroacetic acid and other solvents were supplied by Merck India Ltd (Mumbai). Surat, India-based Span Diagnostics provided aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and TB estimation kits. Thiobarbituric acid and dithiobis nitrobenzoic acid were given by Himedia, Mumbai, India.

Preliminary phytochemical testing

A primary phytochemical analysis was performed on the extracts to figure out the presence of phytoconstituents.[30]

Antioxidant activity

DPPH free radical scavenging activity

A methanolic solution (50 µL) of each sample or positive control at different concentrations was added to 1.95 mL of 1,1-diphenyl-2-picrylhydrazyl (DPPH) solution (6×10–5 mol/L in methanol).[31] Ascorbic acid was utilized as an antioxidant reference, and methanol was utilized as a control. The absorbance at 515 nm was estimated following 30 min of incubation at room temperature. The absorbance (A) of the control and samples was measured, and the DPPH scavenging operation (SA) was computed as follows:

SA% = [(AcontrolAsample)/Acontrol] × 100

The IC50 value (µg/mL) is the concentration at which the scavenging activity was 50%.

Experimental animals

Male wistar albino rats weighing 130±10 g aged 12–16 weeks were selected from the departmental colony and housed in well-ventilated stainless steel cages at room temperature (24±2°C) in hygienic conditions under natural light and dark schedules and fed a standard laboratory diet. Food and water were provided on an ad libitum basis. The experiments were conducted at PBRI (Reg. No. 824/PO/Ere/S/15/CPCSEA). As per OECD guidelines, following approval from the Institute’s Animal Ethics Committee (IAEC).

Acute toxicity study

According to the OECD 423 rule, Wistar albino rats were divided into four classes of three animals each. P. persicaria L. at doses of 5, 50, 300, and 2000 mg/kg was administered orally to various groups of animals. All animals were kept under observation for 14 days to look for toxic symptoms.

Experimental design

The trail was carried out in five groups consisting of 6 rats each. Group I, served as normal control recived the vehicle (5% gum acacia; 1 mL/kg; p.o.). Group II served as a toxicant control, recieved only 1.5 mL/kg of CCL4. Orally, Animals in Group III, served as standard group were given 100 mg/kg of standard silymarin. Animals in Group IV and Group V were given an oral dose of P. persicaria L. aqueous extract suspended in 5% aqueous gum acacia at doses of 200 mg/kg and 400 mg/kg respectively. The treatment was given once a day for a period of 14 days. On the 14th day, 30 min after the extract administration, animals in Groups III–V were given 1.5 mL/kg of CCl4 (1:1 of CCl4 in olive oil i.p.).

Evaluation of hepatoprotective properties

After the experimental procedure was completed, blood was collected from retro-orbital plexus of animals with a fine sterilized glass capillary under mild ether anesthesia and extracted in glass tubes to isolate the serum. The serum was obtained by allowing blood samples to coagulate for 30 min at 37°C.

  Results Top

Phytochemical examination

Phytochemical analysis revealed that the presence of flavonoids, tannins, saponins, terpenoids and alkaloids in the plant root extract [Table-1].
Table 1: Preliminary phytochemical screening of P. persicaria L.

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P. persicaria L. extract antioxidant assay

[Table 2] displays the results. The P. persicaria L. extract has an IC50 =54.48 µg/mL (the concentration needed to prevent radical development by 50%), comparable with the IC50 value of ascorbic acid of 37.62 µg/mL; the extract of P. persicaria L. has a lower IC50 value than that of L-ascorbic acid [Table-2].
Table 2: DPPH scavenging activities of extract of P. persicaria L. and ascorbic acid as control

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Acute toxicity

During the observation period, rats given graduated doses of the P. persicaria L. aqueous extract (5, 50, 300, and 2000 mg/kg) showed no significant changes in breathing, behavior, sensory nervous system responses, gastrointestinal effects, cutaneous effects, and no signs of toxicity such as irritability, altered touch response, abnormal hindquarter tone or body tremors, seizures, straub movement, sedation, increased or decreased urination or defecation, piloerection, or cyanosis. There was no mortality in either of these categories after 24 h of extract administration. Up to a dosage range of 2000 mg/kg, there was no mortality in the acute toxicity sample.

[Table 3] shows ALT, AST, and ALP concentrations in the serum of CCl4-induced liver damage rats after the daily oral administration of aqueous extract of P. persicaria (200 and 400 mg/kg) for 14 days. There was a significant (P ≤ 0.001) increase in the concentration of all these hepatic marker enzymes (ALT, AST, ALP) in the CCl4-induced groups, when compared with the control, whereas the treatment with the aqueous extract of P. persicaria significantly decreased the activity of hepatic marker enzymes. Furthermore, the level of bilirubin increased in the CCl4 group when compared with the normal group. On the contrary, treatment with P. persicaria (200 and 400 mg/kg) shows a significant decrease in the bilirubin level. The standard drug silymarin (100 mg/kg)-treated Group III rats also showed significant (P ≤ 0.001) protection against CCl4-induced liver damage through the above markers.
Table 3: Effects of aqueous extract of P. persicaria L. on carbon tetrachloride-induced hepatotoxicity-related parameters in rats

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Histopathological studies

Histopathology of different treatment types: [Figure 1(a)] shows the normal control group’s liver structure, which includes a central vein and a hepatocyte column (Group I). CCl4 (Group II) toxicity control liver sections revealed extensive changes throughout the lobules, including fatty degeneration, mononuclear inflammatory cell infiltration, and necrosis [Figure 1(b)]. [Figure 1(c)] shows pre-treatment with silymarin (100 mg/kg) in the liver with intact hepatocytes and a completely restored central vein (Group III). [Figure 1(d)] shows tissues with a clogged central vein, necrosis, and fatty modifications that had been pre-treated with P. persicaria L. (200 mg/kg) + CCl4 therapy (Group IV). [Figure 1(e)] shows a typical liver structure with central vein, sinusoid, and hepatocytes in animals treated with 400 mg/kg + CCl4P. persicaria L. aqueous extract (Group V). The parts were stained with H & E (hematoxylin and eosin) before being examined.
Figure 1: (a) Normal liver cell (Group I). (b) Toxicant (Group II). (c) Completely resorted near normal (Group III). (d) Lesser damage of hepatocytes and low necrosis (Group IV). (e) Preserved cytoplasm and lesser fatty changes (Group V)

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  Discussion Top

Liver is responsible for the majority of metabolic processes, and its disruption causes liver injury.[32] Many hepatotoxins cause oxidative stress, which naturally generated antioxidants that neutralize.[33] Over the last few decades, the search for naturally occurring antioxidants has become a major scientific issue. Ayurveda suggests a number of herbal formulations for the treatment of liver diseases.[34] Cytotoxicity and hepatoprotective activities of plant extracts have recently gained prominence for primary level screening. HepG2 cells are regarded as a reasonable model for researching in vitro xenobiotic metabolism and liver damage as they retain the bulk of specialized capabilities found in normal human hepatocytes.[35] Our findings, when combined with those of others,[35],[36] demonstrated that CCl4 generated a time-dependent formation of ROS and subsequent lipid peroxidation in HepG2 cells, with the highest occurring after a 24-h incubation period.

The hepatotoxic agent CCl4 causes selective toxicity to liver cells as a result of metabolic activation, allowing them to maintain semi-normal metabolic function. It also causes harmful morphological changes in the cell membrane causing cell death.[2] The hepatic cells comprise larger amounts of AST and ALT in the cytoplasm, and AST specifically resides in mitochondria.[37] Plasma leakage occurs as a result of hepatic cell injury, resulting in elevated levels of hepatospecific enzymes in the blood.[38]

Elevated serum enzyme levels in the liver are suggestive of cell leakage and cellular membranes that have lost functional dependability.[39] Hepatic cell's ability to detect serum ALP and bilirubin levels is exploited. When compared with the control, the organization of CCl4 induced a significant (P ≤ 0.001) increase in enzyme levels, such as AST, ALT, ALP, and total bilirubin. On administration of the P. persicaria L. extract, there was a significant (P ≤ 0.001) recovery of these enzyme levels [Table 3]. This is in line with the commonly held idea that after hepatic parenchymal regeneration and hepatocyte restoration, serum transaminase levels revert to normal.[40]

In the current study, pre-treatment of CCl4-intoxicated rats with aqueous extract roots of P. persicaria L. (200 and 400 mg/kg) resulted in a considerable reversal of these parameters toward normal. P. persicaria L. extracts had effects similar to conventional silymarin activity. The hepatoprotective effect of P. persicaria L. extract against CCl4 damage is supported by this finding. Furthermore, when compared with unaffected rats, CCl4-treated rats showed greater serum bilirubin levels. The most sensitive factor that demonstrates jaundice’s strength is an increase in serum bilirubin levels.[39] The ability of the aqueous extract (200 and 400 mg/kg) to lower total bilirubin levels in the serum of intoxicated rats suggests that it may be effective in removing bilirubin from the blood when its level is elevated [Table 4].
Table 4: Acute toxicity of aqueous extract of P. persicaria

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Natural antioxidants have received a lot of attention in recent years due to their health advantages.[41] Free radicals are chemical entities that have one or more unpaired electrons, making them exceedingly unstable and capable of causing damage to neighboring molecules by withdrawing electrons to achieve equilibrium.[42] The DPPH free radical scavenging assay is a simple method for detecting antioxidants in plant extracts. When an antioxidant is present, the DPPH radical receives an electron, resulting in a reduction in absorbance.[43] With an increase in the content of P. persicaria L. and ascorbic acid in the current sample from 20 to 100 µg/mL, the percentage of DPPH radical scavenging impact increased. Ascorbic acid had an IC50 of 37.62 µg/mL, whereas the aqueous extract of P. persicaria had an IC50 of 54.48 µg/mL [Table 2].

Toxicology experiments revealed that the oral administration of P. persicaria L. extract is non-lethal (harmless) at acute dosages of 2000 mg/kg. The determination of LD50, which is a single dose at which 50% mortality occurs, is an early screening step in the assessment and evaluation of the poisonous nature of medicinal plants as it helps to establish the safety margin of the medicinal plant under research. Therefore, the approximate LD50 of the aqueous extract of P. persicaria L. was determined to be more than 2000 mg/kg body weight.

According to the histological examinations, CCl4 induced extensive fatty transition, cellular enlargement, invasion, blood vessel obstruction, necrotic foci, disruption of the lobular architecture, blood vessel obstruction, nuclear degeneration in some locations, and fibrosis.[44] The current findings, which demonstrated significant changes in the hepatic cell architecture after CCl4 induction, back up this theory. P. persicaria L. therapy improved all forms of hepatocyte degeneration, including necrosis and inflammatory cell invasion. According to the reports, there was only modest fat vacuole deposition and minor fibrous tissue. This offered additional evidence that the extract of P. persicaria, in addition to its antioxidant and hepatoprotective capabilities, could have an antifibrotic effect by increasing liver function enzymes and oxidative stress indicators. The hepatoprotective antioxidant effects of P. persicaria L. were found to be highly effective when compared with those of silymarin, prompting a further phytochemical investigation of its bioactive ingredients.

The extract contains flavonoids and phenolic compounds that have been shown to have antioxidant and hepatoprotective effects in preliminary phytochemical research. Saponins in the P. persicaria L. aqueous extract are thought to play a significant role as antioxidants in the prevention of oxidative hepatic harm. Additionally, the flavonoids and saponins in the P. persicaria L. aqueous extract may be able to balance ROS by reacting with them and oxidizing them to more stable and less reactive radicals. Secondary metabolites such as phenols, flavonoids, and alkaloids[45] are important secondary metabolites with a wide range of pharmacological applications [Table 1].

Antioxidants found in medicinal plants are typically linked to protection against oxidative stress and hepatotoxicity.[46] As a result, we hypothesized that P. persicaria, a medicinal plant, possesses the antioxidant capacity and hence represents a possible hepatoprotective agent.

  Conclusion Top

The current study demonstrated that an aqueous extract of P. persicaria L. roots had a hepatoprotective effect in Wistar rats when exposed to carbon tetrachloride. The antioxidant activity of P. persicaria’s active component plumaged could explain how the plant defends against CCl4-induced changes. As a result, more research is needed to figure out which elements are responsible for hepatoprotective function and how they work.


The authors are exceedingly grateful to the supervisor and research center for their invaluable assistance and advice in this type of research activity, as well as for providing all laboratory resources.

Financial support and sponsorship


Conflicts of interest

The authors state that they have no conflicts of interest.

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  [Figure 1]

  [Table 1], [Table 2], [Table 3], [Table 4]


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