Green tea modulates reserpine toxicity in animal models

Abstract

-Reserpine, a natural product extracted from or -ria, is a known dopamine depleter that inhibits several neurotransmitters. Reserpine has been used clinically to control hypertension, schizophrenia, insomnia and insanity. The use of this drug, however, has been limited because of its side effects which include oxidative damage to organs, including the liver. Green tea catechins are potent antioxidants that have the potential to counteract reserpine induced oxidative stress. This study investigated the merits of administering green tea concurrently with reserpine to prevent oxidative hepatic damage in Sprague-Dawely (SD) rats. Reserpine was found to cause hepatic damage, with elevated levels of oxidative stress markers, such as Thiobarbituric Acid Reactive Substances (TBARS), transaminases and cholesterol. Reserpine also induced hepatic ultra-structural damage in the cytoplasmic membrane, nuclear envelope, endoplasmic reticulum (rER), ribosomal stripping and mitochondria. Electron microscopy examination showed revival of liver cells as a result of green tea extract administration to experimental rats.

Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells

“…Results obtained in the present study supported the data previously obtained on hepatic recovery by green tea. Indicating a remarkable degree of recovery from in oxidative stress (Al-Bloushi et al, 2009).…”

“…Its antioxidant properties help scavenge the destructive free radicals in the body (Yoko and Santosh, 2005). Recent studies suggest that green tea has positive effects on several body organs in laboratory animals (Hisamura et al, 2006;Adhami and Mukhtar, 2007;Asfar et al, 2007;Safer et al, 2007;Khan et al, 2007;Al-Bloushi et al, 2009). The effects of which have been well-documented when used for the purpose of tissue damage recovery (Adhami and Mukhtar, 2007;Asfar et al, 2007;Safer et al, 2007;Al-Bloushi et al, 2009), or when synergistically used with cofactors like CoQ9 in rats in lowering LDL-Cholesterol (Upaganlawar et al, 2006;Afzal et al, 2007).…”

“…Reserpine depletes biogenic amines such as noradrenalin, dopamine and serotonin and is a potent oxidant (Osubor and Nwanze, 1994;Metzger et al, 2002). It has deteriorating effects on rat liver structure and function Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells (Al-Bloushi et al, 2009). We have undertaken to assess the revival of kidney cells as a result of green tea administration to rat and the status of thiobarbituric acid reactive substances (TBARS).…”

Green tea polyphenols and their potential role in health and disease

“…Specifically, hepatic fibrosis is a result of the inhibition of synthesis and degradation of the matrix due to insult occurring in the mesenchymal cells (MSCs) involved in the synthesis of various components of the ECM, including collagen types I-VII (Paz and Shoenfeld 2010). Results from our laboratories show that green tea extract (GTE) plays a beneficial role in controlling the fibrotic effects of reserpine (Al-Bloushi et al 2009). Our results also show that the effect of hepatic fibrosis inducers such as carbon tetrachloride (CCl 4 ) and ethanol may also be avoided by GTE.…”

Curative propensity of green tea extract towards hepatic fibrosis induced by CCl4: A histopathological study

“…The cells responsible for extracellular matrix (ECM) fiber formation are hepatic stellate cells (HSCs), which enhance cell proliferation at the onset of liver injury (6). During our previous studies of the effect of green tea extract (GTE) on the liver, kidney, and stomach, we presented various observations on the role of GTE in altering the deleterious effects of drugs such as reserpine within 30 days of administration (7,8). This encouraged us to study the effect of GTE on the amelioration of hepatic fibrosis caused by carbon tetrachloride (CCl 4 ) (9, Safer et al, Third Kuwait International Pharmacy Conference, Kuwait, 2011), which induces hepatic fibrosis through oxidative stress.…”