Mulberry extracts are antidiabetic and antihyperlipidemic, as well as preventive of cardiovascular
disease. The current study investigates the protective mechanisms of mulberry water extracts (MWEs)
in carbon tetrachloride (CCl4)-induced hepatic injury. Oral administration of MWEs significantly reduced
the lipid peroxidation triggered by CCl4, as shown by the reduced production of thiobarituric acidreactive substance (TBARS). The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were also reduced via cotreatment with MWEs compared with
CCl4treatment alone. Cotreatment with MWE evidently reduced CCl4-induced liver weight and inhibited
lipid deposition and fibrogenesis. In a similar manner, cotreatment with silymarin, a well-known liver
protective agent, also reversed the CCl4-induced effects, such as reduced TBARS formation, decreased
serum AST, ALT, and ALP levels, blocked lipid accumulation, and liver fibrosis. Furthermore, MWEs attenuated the proinflammatory genes such as cyclooxygenase 2, nuclear factor kappa B, and inducible nitric
oxide synthase expression. The current findings suggest that MWEs such as silymarin exhibit protective
and curative effects against CCl4-induced liver damage and fibrosis via decreased lipid peroxidation and
inhibited proinflammatory gene expression
Mulberry extracts are antidiabetic and antihyperlipidemic, as well as preventive of cardiovasculardisease. The current study investigates the protective mechanisms of mulberry water extracts (MWEs)in carbon tetrachloride (CCl4)-induced hepatic injury. Oral administration of MWEs significantly reducedthe lipid peroxidation triggered by CCl4, as shown by the reduced production of thiobarituric acidreactive substance (TBARS). The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were also reduced via cotreatment with MWEs compared withCCl4treatment alone. Cotreatment with MWE evidently reduced CCl4-induced liver weight and inhibitedlipid deposition and fibrogenesis. In a similar manner, cotreatment with silymarin, a well-known liverprotective agent, also reversed the CCl4-induced effects, such as reduced TBARS formation, decreasedserum AST, ALT, and ALP levels, blocked lipid accumulation, and liver fibrosis. Furthermore, MWEs attenuated the proinflammatory genes such as cyclooxygenase 2, nuclear factor kappa B, and inducible nitricoxide synthase expression. The current findings suggest that MWEs such as silymarin exhibit protectiveand curative effects against CCl4-induced liver damage and fibrosis via decreased lipid peroxidation andinhibited proinflammatory gene expression
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