Effects of Palm Vitamin E on Bone-Formation-Related Gene Expression in Nicotine-Treated Rats

Abstract

The study determines the effects of palm vitamin E on the gene expression of bone-formation-related genes in nicotine-treated rats. Male rats were divided into three groups: normal saline olive oil (NSO), nicotine olive oil (NO), and nicotine palm vitamin E (NE). The treatment was carried out in 2 phases. During the first 2 months, the NSO group received normal saline while the NO and NE groups received nicotine 7 mg/kg, 6 days a week, intraperitoneally. The following 2 months, normal saline and nicotine administration was stopped and was replaced with oral supplementation of olive oil for the NSO and NO groups and oral supplementation of palm vitamin E (60 mg/kg) for the NE group. Both femurs were harvested to determine the gene expression of bone morphogenetic protein-2 (BMP-2), Osterix (OSX), and Runt-related transcription factor 2 (RUNX2). Nicotine significantly downregulated the gene expression. This effect was reversed by palm vitamin E treatment. In conclusion, palm vitamin E may play a role in osteoblast differentiation and can be considered as an anabolic agent to treat nicotine-induced osteoporosis.

Effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 osteoblast-like cells

“…Evidence shows that vitamin E can reverse nicotineinduced toxic effects on bone biochemical markers and osteogenic gene expression [5,6]. These findings were in line with our results, which showed that the negative effects of 5 mM nicotine on ALP/BSP/OC expression significantly decreased in the presence of 5 mM vitamin E to the normal level.…”

“…Furthermore, animal experiments showed that oxidative stress induced by nicotine affected bone metabolism by down-regulating the expression of osteogenic genes [14]. Vitamin E possesses antioxidant properties, and it was shown that it up-regulated osteogenic gene expression in nicotine-treated rats [6] and improved structural, dynamic and cellular histomorphometric parameters of bone [4,5,40,41].…”

“…Nicotine as the main toxic component of cigarette smoke increases oxidative stress due to the formation of free radicals [3]. Animal studies have indicated that oxidative stress due to the effects of nicotine affects bone metabolism and delays bone healing [4][5][6][7]. Reactive oxygen species stimulate osteoclast differentiation [8][9][10] and inhibit the differentiation of osteoblasts [11,12].…”

“…It has been explained that the effects of vitamin E on bone formation are via osteoblast stimulation [20] and suppression of osteoclast differentiation [22]. Thus, vitamin E can be considered as an anabolic agent for treatment of nicotine-induced osteoporosis [6].…”

Potential Role of Tocotrienols on Non-Communicable Diseases: A Review of Current Evidence

“…T3 may also affect the formation and activities of bone cells at gene levels. Utilizing nicotine-induced osteoporosis rat model, Abukhadir et al (2012) reported that PVE increased gene expression related to bone formation such as BMP-2, a growth factors known to induce bone and cartilage formation, as well as Runt-related transcription factor 2 (Runx-2) and osterix (OSX), which play key roles in osteoblast differentiation [165]. In the testosterone deficiency model, annatto T3 enhanced the expression of gene related to bone formation and osteoblast activity, such as alkaline phosphatase (ALP), β-catenin, and collagen type I alpha 1 (COL1α1) [147].…”