Editing Peony root extract
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''Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the mRNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats (P<0.05 or P<0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P<0.05 orP<0.01). In addition, PF significantly inhibited the nuclear factor κB (NF-κB) pathway in the hippocampus of VD rats.'' {{#pmid:26577108|yang2015}} | ''Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the mRNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats (P<0.05 or P<0.01). PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats (P<0.05 orP<0.01). In addition, PF significantly inhibited the nuclear factor κB (NF-κB) pathway in the hippocampus of VD rats.'' {{#pmid:26577108|yang2015}} | ||
| − | ''Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1β. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-α, and IL-1β from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.'' | + | ''Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1β. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-α, and IL-1β from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.'' [3] |
| − | '' We found that PF inhibited the expression of CD69/CD86 and the proliferation of B cells stimulated by LPS. In addition, PF reduced the B-cell differentiation and immunoglobulin production that was stimulated by LPS. Interestingly, PF did not alter B-cell activation and proliferation provoked by anti-CD40 or IL-4. These results indicated for the first time that PF inhibits B-cell activation, proliferation and differentiation by selectively blocking the LPS/TLR4 signaling pathway. Furthermore, our data suggest that PF selectively inhibits inflammation and tissue damage mediated by LPS-activated B cells but does not alter CD40/CD40L- or IL-4-provoked B-cell function in autoimmune diseases treatment, which might aid in protecting patients from secondary infection.'' | + | '' We found that PF inhibited the expression of CD69/CD86 and the proliferation of B cells stimulated by LPS. In addition, PF reduced the B-cell differentiation and immunoglobulin production that was stimulated by LPS. Interestingly, PF did not alter B-cell activation and proliferation provoked by anti-CD40 or IL-4. These results indicated for the first time that PF inhibits B-cell activation, proliferation and differentiation by selectively blocking the LPS/TLR4 signaling pathway. Furthermore, our data suggest that PF selectively inhibits inflammation and tissue damage mediated by LPS-activated B cells but does not alter CD40/CD40L- or IL-4-provoked B-cell function in autoimmune diseases treatment, which might aid in protecting patients from secondary infection.'' [4] |
| − | + | == Discussion threads on the ALSTDI forum == | |
| + | |||
| + | * [http://www.alstdi.org/forum/yaf_postst48193_peony-root-and-paeoniflorin-long-essay.aspx Peony root and paeoniflorin - long essay] | ||
| + | |||
| + | * [http://www.alstdi.org/forum/default.aspx?g=posts&t=45820 Heat shock inducers] | ||
| + | |||
| + | * [http://www.alstdi.org/forum/yaf_postst53948_peony-root.aspx Peony root] | ||
== References == | == References == | ||
| + | |||
| + | [3] | ||
| + | <bibtex> | ||
| + | @article{Nam2013, | ||
| + | abstract = {Chronic activation of microglial cells endangers neuronal survival through the release of various proinflammatory and neurotoxic factors. Paeoniflorin (PF), a water-soluble monoterpene glycoside found in the root of Paeonia lactiflora Pall, has a wide range of pharmacological functions, such as anti-oxidant, anti-inflammatory, and anti-cancer effects. Neuroprotective potential of PF has also been demonstrated in animal models of neuropathologies. Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1$\beta$. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-$\alpha$, and IL-1$\beta$ from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.}, | ||
| + | author = {Nam, Kyong-Nyon and Yae, Che Gyem and Hong, Joung-Woo and Cho, Dong-Hyung and Lee, Joon H and Lee, Eunjoo H}, | ||
| + | doi = {10.1007/s10529-013-1192-8}, | ||
| + | issn = {1573-6776}, | ||
| + | journal = {Biotechnology letters}, | ||
| + | keywords = {Animals,Anti-Inflammatory Agents,Anti-Inflammatory Agents: metabolism,Benzoates,Benzoates: metabolism,Brain,Brain: drug effects,Brain: immunology,Brain: pathology,Bridged Compounds,Bridged Compounds: metabolism,Cell Death,Cell Death: drug effects,Glucosides,Glucosides: metabolism,Hippocampus,Hippocampus: drug effects,Hippocampus: immunology,Hippocampus: pathology,Immunologic Factors,Immunologic Factors: metabolism,Inflammation,Inflammation: pathology,Interleukin-1beta,Interleukin-1beta: metabolism,Lipopolysaccharides,Lipopolysaccharides: immunology,Lipopolysaccharides: toxicity,Microglia,Microglia: drug effects,Microglia: immunology,Monoterpenes,Neuroprotective Agents,Neuroprotective Agents: metabolism,Nitric Oxide,Nitric Oxide: metabolism,Rats,Tumor Necrosis Factor-alpha,Tumor Necrosis Factor-alpha: metabolism}, | ||
| + | mendeley-groups = {peony}, | ||
| + | month = aug, | ||
| + | number = {8}, | ||
| + | pages = {1183--9}, | ||
| + | pmid = {23559368}, | ||
| + | title = {{Paeoniflorin, a monoterpene glycoside, attenuates lipopolysaccharide-induced neuronal injury and brain microglial inflammatory response.}}, | ||
| + | url = {http://www.ncbi.nlm.nih.gov/pubmed/23559368}, | ||
| + | volume = {35}, | ||
| + | year = {2013} | ||
| + | } | ||
| + | </bibtex> | ||
| + | |||
| + | [4] | ||
| + | <bibtex> | ||
| + | @article{Zhang2015, | ||
| + | abstract = {B cells are important in the development of autoimmune disorders through mechanisms involving dysregulated polyclonal B-cell activation, production of pathogenic antibodies, and targeting which reduces inflammation and tissue damage effectively but often leads to patients suffering from secondary infection. Paeoniflorin (PF) is the main substance of the Total glucosides of peony and has been widely used to treat autoimmune diseases for years. However, whether PF affects B cell activity remains unknown. In this study, using purified murine spleen B cells, we analyzed the effects of PF on B-cell function in vitro. We found that PF inhibited the expression of CD69/CD86 and the proliferation of B cells stimulated by LPS. In addition, PF reduced the B-cell differentiation and immunoglobulin production that was stimulated by LPS. Interestingly, PF did not alter B-cell activation and proliferation provoked by anti-CD40 or IL-4. These results indicated for the first time that PF inhibits B-cell activation, proliferation and differentiation by selectively blocking the LPS/TLR4 signaling pathway. Furthermore, our data suggest that PF selectively inhibits inflammation and tissue damage mediated by LPS-activated B cells but does not alter CD40/CD40L- or IL-4-provoked B-cell function in autoimmune diseases treatment, which might aid in protecting patients from secondary infection.}, | ||
| + | author = {Zhang, Jie and Li, Huidan and Huo, Rongfen and Zhai, Tianhang and Li, Haichuan and Sun, Yue and Shen, Baihua and Li, Ningli}, | ||
| + | doi = {10.1016/j.jphs.2015.02.011}, | ||
| + | issn = {1347-8648}, | ||
| + | journal = {Journal of pharmacological sciences}, | ||
| + | mendeley-groups = {peony}, | ||
| + | month = may, | ||
| + | number = {1}, | ||
| + | pages = {8--16}, | ||
| + | pmid = {26041080}, | ||
| + | title = {{Paeoniflorin selectively inhibits LPS-provoked B-cell function.}}, | ||
| + | url = {http://www.ncbi.nlm.nih.gov/pubmed/26041080}, | ||
| + | volume = {128}, | ||
| + | year = {2015} | ||
| + | } | ||
| + | </bibtex> | ||
[[Category:Supplement data pages]] | [[Category:Supplement data pages]] | ||
[[Category:Anti-inflammatory supplements]] | [[Category:Anti-inflammatory supplements]] | ||
