**6. Histopathological studies**

in TBARS level. The standard hepatoprotective drug Silymarin maintained the decreased lipid

Concomitant cellular oxidative stress was manifested by reduced GSH levels and in‐ creased lipid peroxidation. The inverse linear relationship between the ROS level and the GSH level indicated that free radical species were generated by exposure to anti TB drugs which reduced intracellular antioxidant levels. The results indicate that, the herbal drug *Phyllanthus amarus* has very good hepatoprotective effect in liver damage. The results were

Superoxide dismutase and Catalase mutually function as important enzymes in elimination of Reactive oxygen species (ROS). SOD is the major attractive metalloprotein in the antioxidant family. The defensive antioxidant enzyme next to SOD is CAT. CAT is an enzymatic antioxi‐ dant widely distributed in all animal tissues, and the highest activity is found in the red cells and liver. Both are the key component of the antioxidant defense system. In the present study, the observed decrease in SOD and CAT activities were presumably associated with the increased oxidative stress caused by these toxicants that might be due to low level of zinc (a metal constituent of the enzyme SOD) in liver tissue (Arun and Balasubramanian, 2011) Therapy at 200-400 mg/kg b.w. reversed the SOD and CAT activity in the liver tissues and protected from free radical induced oxidative stress. These observations are substantiated by

ATPase is a membrane bound enzyme. Since, phosphatase is a constituent of all the body tissues; it plays an important role in inorganic pyrophosphates activity. ATPase activity may be considered as a marker for assessing hepatocellular damage induced by hepatotoxic agents.

In our experiment, a concurrent fall was found in ATPase in liver after toxicants exposure. It might be due to dysfunctional and dystrophic changes in the mitochondria and cell membrane permeability. This damage was also very clearly visible in histopathological studies after toxicant administration. These observations are substantiated by other authors (Gao and Zhou, 2005; Krithika and Verma, 2009).The effect of the extracts on ATPase was as pronounced with

Liver damage induced by toxicant was associated with a variety of biochemical abnormalities following loss of integrity of the cell membrane or interference with normal hepatocytes

The reason for hepatoprotective effect of the extracts may be due to presence of lignans and

The results of this study showed that common medicinal plant, *P. amarus* even at minimal dose 300mg/kg was found to have beneficial hepatoprotective properties in albino rats as all the

flavonoids which might have scavenged the free radical offering hepato protection.

peroxidation level to the normal limits in the liver.

290 Pharmacology and Nutritional Intervention in the Treatment of Disease

author (Gnanadesigan *et al.,* 2011).(Table 5)

100mg/kg as with 200-400mg/kg b.w.

metabolism and function.

**5. Conclusion**

presented in the Table 4.

(Table 6)

**Figure 1.** Hepatocytes of the normal control group showed a normal lobular architecture of the liver (400 x).

**Figure 2.** Hepatocytes of the INH + RIF+ PZA treated group showed liver cell necrosis and inflammation also observed in the centrilobular region with portal triaditis (400 x).

um tuberculosis strains by DNA sequencing: a randomized trial. Annals of Clinical

Hepatoprotective effect of *Phyllanthus amarus*

http://dx.doi.org/10.5772/57373

293

[4] Eminzade S, Uras F and Izzettin FV. (2008). Silymarin protects liver against toxic ef‐ fects of anti-tuberculosis drugs in experimental animals. Nutrition & Metabolism,

[5] Devaraj VC, Gopala KB, Viswanatha GL, Kamath JV, Kumar S (2011). Hepatoprotec‐ tive activity of Hepax-A polyherbal formulation. Asian Pacific Journal of Tropical Bi‐

[6] Joshi H, Parle M (2007). Pharmacological evidences for antiamnesic potentials of *Phyllanthus amarus* in mice. African Journal of Biomedical Research, Vol. 10; 165 –

[7] Lee S B, Bablanian R and Esteban M. (1996). Regulated expression of the interferoninduced protein kinase p68 (PKR) by vaccinia virus recombinants inhibits the repli‐ cation of vesicular stomatitis virus but not that of poliovirus. Journal of Interferon

[8] Reitman and Frankel. (1957). A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases. Amer. J. Clin. Pathol. 28:

[9] Sharma SK and Krishnamurthy CR (1968). Production of lipidperoxides of brain. J

[10] Misra HP and Fridovich I (1972). The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem. 247: 3170–

[12] Ranawat L, Bhatt J and Patel J. (2010). Hepatoprotective activity of ethanolic extracts of bark of Zanthoxylum armatum DC in CCl4 induced hepatic damage in rats. J. Eth‐

[13] Muriel P, EscobarY (2003). Kupffer cells are responsible for liver cirrhosis induced by

[14] Thirunavukkarasu C, Sakthisekaran D (2003).Influence of sodium selenite on glyco‐ protein contents in normal and N-nitrosodiethylamine initiated and Phenobarbital

[16] Adebisi SA, Oluboyo PO, Okesina AB (2000).Effect of drug-induced hyperuricaemia on renal function in Nigerians with pulmonary tuberculosis. Afr J Med Med Sci.

[15] Zimmerman L (1973).Podiatry and the law.J Am Podiatry Assoc, 63; 691-3.

[11] Aebi H (1984). Catalase in vitro; Methods Enzymol. 105. 121–126

carbon tetrachloride. J. App. Toxicol., 23(2):103-108.

promoted rat liver tumors. Pharmacol Res 48(2):167-73.

Microbiology and Antimicrobials, 8:4.

and Cytokine Research 16, 1073-1078.

5:18.

173.

56-63.

3175.

3-4:297-300.

Neurochem; 15: 147-9.

nopharmacol. 127(3):777-780.

omedicine. 142-146.

**Figure 3.** Hepatocytes of the *P.amarus* treated group showed cuboidal hepatocytes with moderate portal triaditis and their lobular architecture was normal (400 x).
