Publications by authors named "Lu Hong Long"

Article Synopsis
  • Social isolation in mice over a period of 8 weeks led to depressive and anxiety-like behaviors, cognitive impairment, and decreased levels of m6A modifications in the hippocampus, along with reduced expression of the enzyme METTL14.
  • The study quantified m6A levels and analyzed the effects of over-expressing METTL14 using a viral tool, which showed that restoring METTL14 levels improved mood and cognitive functions in socially isolated mice.
  • These findings suggest that m6A modifications and the enzyme METTL14 play a critical role in addressing social isolation-induced behavioral impairments, indicating potential targets for therapeutic strategies in managing related mental health issues.
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Sepsis-associated encephalopathy (SAE) refers to diffuse brain dysfunction caused by sepsis, which is characterized by decreased attention, directional impairment, being prone to irritation, and in severe cases the patient will experience drowsiness and coma. The pathogenesis of SAE mainly includes neuroinflammation, damage of blood-brain barrier, cerebral vascular dysfunction, and neurometabolic changes, among which neuroinflammation is the core pathological process. Microglia are considered to be important immune cells of the central nervous system and play an important role in neuroinflammation.

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Tenacissimoside A (1) and 11alpha-O-benzoyl-12beta- O-acetyltenacigenin B (2), two derivatives of tenacigenin B (3) from the plant Marsdenia tenacissima, reversed multidrug resistance in P-glycoprotein (Pgp)-overexpressing multidrug-resistant cancer cells. The sensitivity of HepG2/Dox cells to the antitumor drugs doxorubicin, vinblastine, puromycin, and paclitexel was increased by 18-, 10-, 11-, and 6-fold by 20 microg/mL (or 25 microM) of 1 and 16-, 53-, 16-, and 326-fold by 20 microg/mL (or 39 microM) of 2, respectively. A preliminary mechanistic study has suggested that 1 might modulate Pgp-mediated multidrug resistance through directly interacting with the Pgp substrate site.

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