Correction to: Recent advances in herbal medicine for treatment of liver diseases
Nilanjan Ghosh, Rituparna Ghosh, Vivekananda Mandal, and Subhash C. Mandal. Recent advances in herbal medicine for treatment of liver diseases. Pharmaceutical Biology, 2011; 49(9): 970–988.
Following publication of this article, an error has been identified with regard to citation and referencing of the article content. The citation should have read as follows:
Page 970, left column:
Treatment options for common liver diseases such as cirrhosis, fatty liver, and chronic hepatitis are often limited in efficacy, carry the risk of adverse effects and are often too costly, especially for the developing world [Tavakoli N et al. Formulation and evaluation of a new herbal tablet from strawberry and grape leaves. Jundushapur. Journal of Natural Pharmaceutical Products 2007;3(1):19–25].
Page 971, left column:
In addition, herbal products are often exempt from rigorous regulations, such as in the US, and prescriptions are usually not required for these inexpensive products. The following review describes the current scientific evidence regarding herbal drugs and the liver, especially in regard to their presumed beneficial effect [Stickel F et al. Herbal medicine in the treatment of liver diseases. Dig Liver Dis 2007 Apr;39(4):293–304].
Page 971, left column:
Hepatotoxicity
Liver is one of the largest organs in the human body that performs numerous interrelated vital functions. Some of the commonly known disorders include viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, autoimmune liver disease, metabolic liver disease, drug induced liver injury, toxin-induced liver injury, etc. As a consequence of chronic liver disease, patient may develop portal hypertension and liver cirrhosis. Liver toxicity mainly occurs due to alcohol, viral and induced by drugs [Negi AS. et al. Recent advances in plant hepatoprotectives: A chemical and biological profile of some important leads. Med Res Rev 2008 Sep;28(5):746–72].
Alcoholic liver disease, including acute alcoholic hepatitis and alcoholic cirrhosis, is a major cause of morbidity and mortality in the Western world. In alcoholic liver disease, oxidative stress is caused by pro-oxidant formation, inadequate intake of antioxidants, antioxidant depletion, and alcohol-mediated inhibition of glutathione synthesis. Acetaldehyde is the most important metabolite of ethanol leading to liver damage. Alcohol-induced liver diseases are mediated by cytokines, which are secreted by liver and other parts of the body (Negi, 2008).
Page 975, right column: [Sood et al. Development of a low cost micropropagation technology for an endangered medicinal herb (Picrorhiza kurroa) of North-Western Himalayas. Journal of Plant Sciences 2009;4:21–31]
Page 981, left column:
Asiatic acid
Asiatic acid (AA) is one of the triterpenoid components of Terminalia catappa L. (Combretaceae) which has antioxidative, anti-inflammatory and hepatoprotective activity [Gao J et al. Mechanism underlying mitochondrial protection of asiatic acid against hepatotoxicity in mice. J Pharm Pharmacol (2006) Feb;58(2):227–33].
Page 981, right column: The following should be in quotations from Gao et al. 2006
“VDACs and inhibiting the process of MPT (Gao et al., 2006). The protective effects of AA and the relative mechanism in the d-GalN + LPS induced hepatotoxicity in hepatocytes and kupffer cells co-cultured system have been explored. The cultures were pretreated with AA for 12 h, followed by d-GalN + LPS exposure for 12 h. AA reduced AST and LDH generation and increased cell viability in a concentration-dependent manner. The effects of AA in leukotriene C4 synthase (LTC4S) expression and cellular redox status including ROS and GSH content were detected. The results showed that d-GalN + LPS induced the increase of ROS followed by extracellular signal-regulated kinase 1/2 (ERK 1/2) and NF-κB activation. Treatment with ERK 1/2 specific inhibitor 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (U0126) abolished the ERK1/2 protein phosphorylation and blunted LTC4S expression. ROS signalling pathway inhibitor pyrrolidine dithiocarbamate (PDTC) inhibited ROS generation and NF-κB activation, which in turn blocked LTC4S expression and attenuated the injury.”
Page 983, right column:
Large sections of patients with liver disease use botanicals. Future efforts will have to implement extensive methodological improvements to separate the real therapeutic value of these agents from unsubstantiated hopes associated with them (Stickel, 2007). The active molecules must be isolated and tested through well-designed experiments and finally in randomized, placebo-controlled studies to enable rational clinical use of the agents (Negi, 2008).
Following publication of this article, an error has been identified with regard to citation and referencing of the article content. The following references should have been included in the reference list:
1. Tavakoli N, Ghodrati M, Ghassemi-Dehkordi N, et al. (2007). Formulation and evaluation of a new herbal tablet from strawberry and grape leaves. Jundushapur. J Nat Pharm Prod 3:19–25.
2. Stickel F, Schuppan D. (2007). Herbal medicine in the treatment of liver diseases. Dig Liver Dis 39:293–304.
3. Negri AS, Kumar JK, Luqman S, et al. (2008). Recent advances in plant hepatoprotectives: A chemical and biological profile of some important leads. Med Res Rev 28:746–72.
4. Sood H, Chauhan RS. (2009). Development of a low cost micropropagation technology for an endangered medicinal herb (Picrorhiza kurroa) of North-Western Himalayas. J Plant Sci 4:21–31.
5. Gao J, Chen J, Tang X, et al. (2006). Mechanism underlying mitochondrial protection of asiatic acid against hepatotoxicity in mice. J Pharm Pharmacol 58:227–33.