Reciprocal regulation of SIRT1 and AMPK by Ginsenoside compound K impedes the conversion from plasma cells to mitigate for podocyte injury in MRL/ mice in a B cell-specific manner.

Background: Deposition of immune complexes drives podocyte injury acting in the initial phase of lupus nephritis (LN), a process mediated by B cell involvement. Accordingly, targeting B cell subsets represents a potential therapeutic approach for LN. Ginsenoside compound K (CK), a bioavailable component of ginseng, possesses nephritis benefits in lupus-prone mice; however, the underlying mechanisms involving B cell subpopulations remain elusive.

Curcumin Compensates GLP-1 Deficiency via the Microbiota-Bile Acids Axis and Modulation in Functional Crosstalk between TGR5 and FXR in ob/ob Mice.

Scope: Glucagon-like peptide-1 (GLP-1) deficiency occurs in obesity-related pathologies due to defects in the intestinal lumen. And expanding the L-cell population has emerged as a promising avenue to elevate GLP-1 secretion to tackle metabolic disorders. Curcumin (Cur), the principal active component of spice turmeric, possesses well-established anti-obesity properties.

Fasudil compensates podocyte injury via CaMK4/Rho GTPases signal and actin cytoskeleton-dependent activation of YAP in MRL/lpr mice.

Deposition of immune complexes in the glomerulus leads to irreversible renal damage in lupus nephritis (LN), of which podocyte malfunction arises earlier. Fasudil, the only Rho GTPases inhibitor approved in clinical settings, possesses well-established renoprotective actions; yet, no studies addressed the amelioration derived from fasudil in LN. To clarify, we investigated whether fasudil exerted renal remission in lupus-prone mice.

Ginsenoside compound K increases glucagon-like peptide-1 release and L-cell abundance in db/db mice through TGR5/YAP signaling.

Background: Incretin impairment refers to L-cell-derived glucagon-like peptide-1 (GLP-1) deficiency, commonly observed in patients with type 2 diabetes mellitus (T2DM). Promoting the enteroendocrine L-cell population to elevate GLP-1 secretory capacity represents a potential therapeutic strategy for T2DM. It has been established that ginsenoside compound K (CK) could stimulate GLP-1 secretion; however, the underlying mechanisms remain elusive.

Compound K attenuates hyperglycemia by enhancing glucagon-like peptide-1 secretion through activating TGR5 via the remodeling of gut microbiota and bile acid metabolism.

Background: Incretin impairment, characterized by insufficient secretion of L-cell-derived glucagon-like peptide-1 (GLP-1), is a defining step of type 2 diabetes mellitus (T2DM). Ginsenoside compound K (CK) can stimulate GLP-1 secretion; however, the potential mechanism underlying this effect has not been established.

Methods: CK (40 mg/kg) was administered orally to male db/db mice for 4 weeks.

CT Imaging Characteristics and Influence Factors of Renal Dialysis-Associated Peritoneal Injury.

Peritoneal dialysis (PD), as one of the main renal replacement modalities for end-stage renal disease, gets the advantages of better protection of residual renal function and better quality of survival. However, ultrafiltration failure after peritoneal injury is an important reason for patients to withdraw from PD treatment. Peritonitis is a major complication of peritoneal dialysis, which results in an accelerated process of peritoneal injury due to direct damage from acute inflammation and local release of cytokine TGF-.