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紫草素shikonin改善熱中暑大鼠 之多重器官功能異常及其機轉探討

為了解決LINE Mac dmg的問題，作者石豐榮 這樣論述：

全球暖化所造成的影響與日俱增，像是歐洲熱浪、熱島效應等，逐年升高的氣溫，使夏季的全世界壟罩在熱壓力下，熱壓力會造成熱痙攣或熱衰竭等，甚至會造成熱中暑 (heat stroke；HS)。生物體在處於熱壓力的環境下，會產生一種名為heat shock protein 70 (Hsp70) 的保護蛋白，在環境壓力下，會被大量誘導產生，以幫助蛋白質正常折疊，防止變性，更有文獻指出與發炎作用、自噬作用、細胞凋亡有密切關係。除此之外，heme oxygenase-1 (HO-1) 也會被誘導產生，HO-1為人體的抗氧化酶，也是一種熱休克蛋白 (Hsp32)，能幫助生物體適應環境壓力，也被認為能直接抑制促

炎細胞激素的釋放並誘導生成抗發炎細胞激素，進而達到改善發炎的效果。文獻指出，在諸多中草藥的萃取化合物中，Shikonin (紫草素)在誘導Hsp70的能力，獨占鰲頭，因此本研究是想探討預先給予shikonin後，從誘導大鼠熱中暑的動物模式是否可改善存活率，以及是否能透過抑制發炎及抑制氧化壓力的產生來預防熱中暑造成之多重器官傷害。動物實驗分為以下四組：(1) 控制組 (CTL group)：實驗前15小時，腹腔注射藥物溶劑0.1% dimethyl sulfoxide (DMSO)；(2) 單獨給予shikonin組 (SHK group)：實驗前15小時，腹腔給予shikonin 10 mg/

kg (溶於0.1% DMSO)；(3)熱中暑組 (HS group)：實驗前15小時，腹腔給予0.1% DMSO，並將大鼠放置於42 °C的烘箱中，待其核心溫度達42.8 °C時取出，以此來誘導熱中暑；(4)熱中暑治療組 (SHK + HS group)：實驗前15小時，腹腔注射shikonin 10 mg/kg，之後觀察5個小時，紀錄各組大鼠核心體溫、血壓及心跳變化。實驗結果顯示：預先給予shikonin 能夠明顯提高大鼠熱中暑後5小時的存活率，也會明顯改善熱中暑大鼠體溫調控異常及低血壓情形，明顯降低血中細胞激素IL-1β濃度、肝功能指標 GOT 及GPT、腎功能指標 creatinine

、骨骼肌損傷指標 creatine phosphokinase，以及細胞損傷指標 LDH 濃度，血中血小板數目降低情形也顯著改善。此外，和 HS 組相較，預先給予shikonin可以明顯誘導肝臟 Hsp70及HO-1的生成，降低IL-1β 表現量，降低細胞凋亡相關蛋白Bax/Bcl-2 ratio值，而LC3II/LC3I ratio值以及Atg12-Atg5 complex的生成明顯低於 HS 組。在肺臟部分，預先給予shikonin可以降低IL-1β表現量，抑制發炎反應。由以上實驗結果顯示，shikonin可改善熱中暑大鼠多重器官功能異常及提高存活率，此保護作用可能與其產生抗發炎與抗凋亡作

用有關，亦可能降低自噬作用過度活化所引發之細胞死亡，詳細機轉待未來進一步探討。

鈣離子信號傳導於細胞連結動態所扮演的角色

為了解決LINE Mac dmg的問題，作者Ivan Limanjaya 這樣論述：

BackgroundDuring spermatogenesis, transient permeability of blood-testis barrier achieved through tight junctional dynamics permits spermatocytes to translocate towards the luminal side of seminiferous tubule. Previous studies indicated that L-selectin regulates this tight junctional dynamics throu

gh its downstream effector Rho GTPase and that binding of L-selectin ligand to its receptors in Sertoli cells leads to influx of calcium. The relationship between this calcium influx and Rho GTPase, however, remains to be elucidated.MethodologyUsing fluorescent dye, real-time imaging on ASC-17D cell

s was performed to observe calcium influx following stimulation with an array of ligands for selectins under various conditions. Active small GTPases pull down assay followed by western blot was also performed to further investigate the relationship between calcium influx and activation of Rho GTPas

es.ResultConsistent with results from previous studies, we confirmed the presence of L-type voltage-operated Ca2+ channel-mediated calcium influx following L-selectin stimulation. In accordance with our hypothesis, we also successfully demonstrated increased expression levels of activated Rho and Ra

c1 as the direct consequence of L-selectin-induced calcium influx.ConclusionActivation of L-selectin induces calcium influx through the L-type VOCC which consequently activates Rho and Rac1 in ASC-17D cells.Our findings lead to better understanding of the L-selectin regulated tight junctional dynami

cs. Further continuation of this study might materialise through the investigation of the topological rearrangement of tight junctions following L-selectin-mediated calcium influx.