Objective Folate (vitamin B 9 ) plays key roles in cell growth and proliferation through regulating the synthesis and stabilization of DNA and RNA, and its deficiency leads to lymphocytopenia and granulocytopenia. However, precisely how folate deficiency affects the distribution of a variety of white blood cell subsets, including the minor population of basophils, and the cell specificity of the effects remain unclear. Therefore, we examined the effects of a folate-deficient diet on the circulating number of lymphocyte subsets [T-lymphocytes, B-lymphocytes, and natural killer (NK) cells] and granulocyte subsets (neutrophils, eosinophils, and basophils) in rats. Methods Rats were divided into two groups, with one receiving the folate-deficient diet (FAD group) and the other a control diet (CON group). All rats were pair-fed for 8 weeks.Results Plasma folate level was dramatically lower in the FAD group than in the CON group, and the level of homocysteine in the plasma, a predictor of folate deficiency was significantly higher in the FAD group than in the CON group. The number of T-lymphocytes, B-lymphocytes, and NK cells was significantly lower in the FAD group than in the CON group by 0.73-, 0.49-, and 0.70-fold, respectively, indicating that B-lymphocytes are more sensitive to folate deficiency than the other lymphocyte subsets. As expected, the number of neutrophils and eosinophils was significantly lower in the FAD group than in the CON group. However, the number of basophils, the least common type of granulocyte, showed transiently an increasing tendency in the FAD group as compared with the CON group. Conclusion These results suggest that folate deficiency induces lymphocytopenia and granulocytopenia in a cellspecific manner.
The dietary constituent, resveratrol, was recently identified as a transient receptor potential ankyrin 1 (TRPA1) antagonist, voltage-dependent sodium ion (Na ) channel, and cyclooxygenase-2 (COX-2) inhibitor. The aim of the present study was to investigate whether pretreatment with resveratrol attenuates acute inflammation-induced sensitization of nociceptive processing in rat spinal trigeminal nucleus caudalis (SpVc) and upper cervical (C1) dorsal horn neurons, via c-fos immunoreactivity. Mustard oil (MO), a TRPA1 channel agonist, was injected into the whisker pads of rats to induce inflammation. Pretreatment with resveratrol significantly decreased the mean thickness of inflammation-induced edema in whisker pads compared with those of untreated, inflamed rats. Ipsilateral of both the superficial and deep laminae of SpVc and C1 dorsal horn, there were significantly more c-fos-immunoreactive SpVc/C1 neurons in inflamed rats compared with naïve rats, and resveratrol pretreatment significantly decreased that number relative to untreated, inflamed rats. These results suggest that systemic administration of resveratrol attenuates acute inflammation-induced augmented nociceptive processing of trigeminal SpVc and C1 neurons. These findings support resveratrol as a potential therapeutic agent for use in alternative, complementary medicine to attenuate, or even prevent, acute trigeminal inflammatory pain.
Although lutein is known to inhibit chronic inflammation, its effect on acute inflammation‐induced nociceptive processing in the trigeminal system remains to be determined. The aim of the present study was to investigate whether pretreatment with lutein attenuates acute inflammation‐induced sensitization of nociceptive processing in rat spinal trigeminal nucleus caudalis (SpVc) and upper cervical (C1) dorsal horn neurons, via c‐Fos immunoreactivity. Mustard oil, a transient receptor potential ankyrin‐1 channel agonist, was injected into the whisker pads to induce inflammation. Pretreatment of rats with lutein resulted in significant decreases in the inflammation‐induced mean times of face grooming and the thickness of inflammation‐induced edema in whisker pads relative to those features in inflamed rats (i.e., rats with no lutein pretreatment). In both the ipsilateral superficial and deep laminae of the SpVc and C1 dorsal horn, there were significantly larger numbers of c‐Fos‐positive neurons in inflamed rats than in naïve rats, and lutein pretreatment significantly decreased that number relative to inflamed rats. These results suggest that systemic administration of lutein attenuates acute inflammation‐induced nocifensive behavior and augmented nociceptive processing of SpVc and C1 neurons that send stimulus localization and intensity information to higher pain centers. These findings support lutein as a potential therapeutic agent for use as an alternative, complementary medicine to attenuate, or even prevent, acute inflammatory pain.
We examined the role of hepatocyte growth factor (HGF) in the chondrogenesis and endochondral ossifi cation in the forelimbs of mouse embryos by use of immunohistochemistry and organ culture system. In the forelimbs of embryonic day 14 (E14) embryos, intense immunoreactivity for HGF was localized to the chondrocytes located in the proliferative and early hypertrophic zones, and moderate to weak immunoreactivity in the resting and late hypertrophic zones of bone anlagen. Immunoreactivity for the HGF receptor, c-Met, was also localized to the chondrocytes in the resting, proliferative and early hypertrophic zones. In the explants of forelimb buds from E10 embryos cultured for 8 days, exogenous HGF added to the culture media enhanced proliferation of chondrocytes in the forelimb bone anlagen. In contrast, the antisense oligodeoxyribonucleotide (ODN) for HGF as well as the specifi c HGF antagonist NK4 inhibited proliferation of chondrocytes and caused hypertrophic change and collagen X production, the signs of chondrocyte differentiation, in the arm bone anlagen. Furthermore, the antisense ODN and antagonists for HGF caused a complete lack in the formation of cartilaginous hand and digital bone anlagen. These results suggested that HGF functions in stimulating chondrogenesis and preventing endochondral ossifi cation in the forelimbs of mouse embryos.
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