Sugar coated liposomal flavonoid: A unique formulation in combating carbontetrachloride induced hepatic oxidative damage

Abstract

Rats were administered a single dose of plant origin phenolic antioxidant Quercetin (QC) in free, liposome encapsulated and galactosylated liposome encapsulated forms 2 h prior to hepatotoxic dose of carbontetrachloride (CCl4, 40% v/v in olive oil, 1 ml/kg b.wt). Among those three different forms of QC tested, only galactosylated liposomal QC provided significant protection against CCl4 induced hepatic oxidative damage. After 24 h of injection (S.C.) hepatic cells of rats were found susceptible to CCl4 induced oxidative damage and it was monitored by the increased amount of conjugated diene in hepatic membrane. The two-fold increase in conjugated diene by the induction of CCl4 was decreased upto normal level by galactosylated liposomal QC pre-treatment. Carbontetrachloride induced membrane damage in hepatic cells and it was judged by the blood serum pathological and liver tissue histopathological examination. Membrane damage by the induction of CCl4 was further evaluated by the decreased level of plasma membrane (PM) bound enzyme Na+/K+ ATPase activity and it was increased only by the pre-treatment of galactosylated liposomal QC. Carbontetrachloride induced a substantial decrease both in enzymatic and molecular endogenous antioxidant levels in hepatic cells.The depression in antioxidant system in hepatic cells was completely prevented by a single dose of galactosylated lipsosomal QC prior to CCl4 treatment. Liver uptake of QC was estimated after 2 h of the flavonoid injection (8.9 micromol/kg body weight) (free or liposomal forms) and 85% of the injected QC was found in liver in the case of galactosylated liposomal QC. Whereas only 25% of the injected dose was detected in liver when an identical amount of free QC was injected. Carbontetrachloride also induced an alteration in membrane fluidity and it was evaluated by a decrease in membrane micro-viscosity. Free QC pre-treatment resulted in no protection against CCl4 induced increase in hepatic membrane fluidity, whereas galactosylated liposomal QC exerted a significant protection against the increase. Results of this study revealed that QC in galactosylated liposome could exert a significant protection against CCl4 induced hepatocellular injury.

Nanoencapsulation of quercetin enhances its dietary efficacy in combating arsenic-induced oxidative damage in liver and brain of rats

“…The protective role of quercetin in galactosylated liposomes against carbon tetrachloride-induced hepatocellular damage has been shown in our previous work (Mandal and Das, 2005). Herein, we demonstrated the increased neuroprotective effect of nanocapsulated quercetin compared to its free form against arsenite-induced oxidative damage.…”

“…The residue was dissolved in 0.2 ml of HPLC grade methanol. Next, 20 µl of the solution was injected on an HPLC column, and the quantification of quercetin was performed spectrophotometrically (Mandal and Das et al, 2005). The quercetin encapsulation efficiency of nanocapsules was investigated; they contained 98.5% of the added quantity.…”

Hepatoprotective and neuroprotective activity of liposomal quercetin in combating chronic arsenic induced oxidative damage in liver and brain of rats

“…Arsenic has a direct toxic effect on cellular respiration in liver mitochondria with an evidence of oxidative stress and hepatic collagenesis in human (Yamauchi et al 2002;Mandal and Das 2005). Fibrogenesis is expressed by an increase in the hepatic hydroxyproline levels (Testa et al 1993).…”

Vesicular (liposomal and nanoparticulated) delivery of curcumin: a comparative study on carbon tetrachloride–mediated oxidative hepatocellular damage in rat model

“…Our group has previously demonstrated that galactosegrafted liposome encapsulating an antioxidant can provide significant protection against CCl 4 -mediated fatty liver damage or steatosis. 28 We have taken this study forward and compared the protective efficacy of curcumin-loaded polymeric nanoparticles with curcumin-loaded liposomes. Liposomes have several disadvantages for oral delivery as the lipid bilayer cannot withstand the harsh conditions in the GI tract.…”

“…Microviscosity (r) was calculated using the equation, r = (I II -I ⊥ )/(I II + 2I ⊥ ). 28 succinate dehydrogenase (sDh) and nicotinamide adenine dinucleotide (NaDh) oxidase activity SDH and NADH oxidase activities were evaluated from liver submitochondrial particles. In brief, PMS-mediated 33 By measuring the rate of NADH oxidation spectrophotometrically at 340 nm, glutathione reductase (GR) was assayed.…”