14 • Probe •Vol LXII • No. 3 • May–Aug 2023 Preclinical Evidence Liv.52® (SYRUP, TABLET) Liv.52 is a hepatospecific formulation, designed for the treatment and management of liver disorders. Liv.52 has a wide spectrum of therapeutic applications. Liv.52 restores the metabolic efficiency of the liver, minimizes damage to the hepatic parenchyma, and accelerates the rate of recovery in various liver disorders such as infectious hepatitis and alcoholic liver diseases. Liv.52 is a valuable adjuvant during prolonged illness. In anorexia, Liv.52 improves appetite, digestion, and assimilation. Effect of Liv.52® on Hepatic Enzymes Aim To examine the effect of Liv.52 and the extract of Solanum nigrum on the growth rate of rats; hepatic mitochondrial, microsomal, and lysosomal enzymes; and hexobarbital sleeping time, and also to investigate whether Liv.52 offers any protection against the hepatotoxicity of carbon tetrachloride (CCl4) Materials and Methods The S nigrum extract was prepared by homogenizing 100 g of S nigrum leaves in distilled water (10% homogenate, w/v). It was kept at 80°C for 1 hour and centrifuged. The clear supernatant was then concentrated to dryness in vacuo. Male weanling rats (Druckrey strain) were divided into 3 groups: group 1 received Liv.52 (0.125 mL/kg body weight/d), group 2 received the S nigrum leaf extract (equivalent to its corresponding amount in Liv.52), and group 3 (control) received normal saline for 11 weeks. All the rats had free access to a standard pellet diet and water, and 2 rats were housed in one cage. Their body weight was recorded every week. To measure the hexobarbital sleeping time, the animals were intraperitoneally administered 125 mg of sodium hexobarbital per kg of body weight. Sleeping time was recorded as the time between losing and restoring the righting reflex. Six rats each from the control and Liv.52 groups received a sublethal dose of CCl4 (0.7 mL/kg body weight) intraperitoneally for 2 days. All animals were then fasted for 24 hours and were killed after 48 hours by decapitation. The livers were immediately removed and rinsed with cooled normal saline, and 10% homogenate (w/v) in 0.25 M sucrose was prepared. DNA was extracted from a 2-mL aliquot of the homogenates using the Schneider method and was estimated using diphenylamine reaction. Results Liv.52-fed rats showed significantly better growth at the initial phase (weeks 3–8) compared with those administered the extract of S nigrum or controls; however, by the final phases (weeks 8–11), the body weights of rats in all groups were almost the same. The liver weight in all 3 groups was the same, but the liver protein level in the Liv.52-treated rats increased compared with the S nigrum–treated rats or control rats (Figure). According to DNA estimations, it was evident that there was no liver shrinkage (2.95 and 2.90 mg DNA/g of the liver in control rats and Liv.52-fed rats, respectively). The hexobarbital sleeping time reduced in the Liv.52-treated group (42 ± 6 min) compared with the control and S nigrum–fed group (63 ± 8 and 59 ± 4 min, respectively). The S nigrum–fed rats and Liv.52-treated rats had higher levels of succinate dehydrogenase, cytochrome c
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