In recent years, there has been a pronounced tendency to increase in the incidence of drug-induced liver damage due to the growing expansion of the pharmaceutical market, which is also observed in the case of incorrect administration of nonsteroidal anti-inflammatory drugs (NSAIDs). In this case, the violation of the functional state of the body has a negative effect on synthetic processes, which in combination with the protein system of tissues significantly affects the metabolic homeostasis of the body. Therefore, the aim of the study was to determine marker changes in the plasma protein spectrum in laboratory rats with diclofenac-induced hepatitis and the effectiveness of reparative therapy based on milk phospholipids. The drug form of toxic hepatitis in laboratory animals was induced according to the author’s model by oral administration of diclofenac sodium (NSAID group) at a dose of 12.5 mg/kg, once a day for 14 days. Thus, in rats with toxic hepatitis there was a probable decrease in plasma total protein content by 15.6% compared with control, indicating a violation of protein-synthesizing function of the liver. With the introduction into the body of clinically healthy and sick animals of the liposomal form of the bioadditive "FLP-MD" based on milk phospholipids, the level of total protein in blood plasma corresponded to control values. As a result of the study of the plasma protein spectrum of Wistar rats, the four most sensitive indicators, which undergo significant probable changes in absolute and relative units of measurement with the development of toxic diclofenac-induced hepatitis, are protein fractions with molecular weights of 180–190, 150–170, 60 and 54–58 kDa and four markers of the effectiveness of restoring the protein-synthesizing function of the liver with the use of corrective therapy, in particular, bioadditives "FLP-MD" – 900, 180–190, 68–70 kDa and the value of A/G ratio, which is important for implementation in applied veterinary medicine, especially in the diagnosis of NSAID hepatopathy, supplementing the picture of its pathogenesis at the molecular level and testing the effectiveness of newly created drugs of hepatoprotective profile.