Blockade of p38 mitogen-activated protein kinase pathway ameliorates delayed gastric emptying in streptozotocin-induced diabetic rats.

Background And Aim: Gastrointestinal dysfunction is one of the major complications of diabetes. The roles of inflammation in diabetes and its associated complications are increasingly recognized. p38 mitogen-activated protein kinase (MAPK) has been shown to be involved in the production of pro-inflammatory mediators.

[Blood pressure variability correlates with target-organ damage in elderly patients with hypertension].

Objective: To investigate the relationship between blood pressure variability (BPV)and target-organ damage in elderly patients with hypertension.

Methods: A total of 197 elderly patients were included in the study. The participants were divided into two groups: those with hypertension (n=146) and those without hypertension (Control, n=51).

Tetrandrine suppresses amyloid-β-induced inflammatory cytokines by inhibiting NF-κB pathway in murine BV2 microglial cells.

Microglial cells play an important role in mediating neuroinflammation in Alzheimer's disease (AD) by production of a series of proinflammatory mediators and clearance of Aβ peptides and senile plaques. Tetrandrine, a bisbenzylisoquinoline alkaloid isolated from the Chinese herb Radix Stephania tetrandra, has been demonstrated to decrease the expression of proinflammatory mediators by inhibition of NF-κB activation. Here we investigated whether tetrandrine may affect the phagocytosis of microglia and the expression of cytokines and NF-κB in murine BV2 microglial cells.

PI3K/Akt signaling pathway is involved in the pathogenesis of ulcerative colitis.

Objective: The purpose of this study was to investigate the role of the PI3K/Akt signaling pathway in the pathogenesis of ulcerative colitis (UC).

Materials And Methods: Mucosal biopsy specimens from 54 active UC cases and adjacent normal tissues from 18 colon cancer cases were investigated. Twenty-eight Balb/c mice were randomly divided into four groups.

Tetrandrine attenuates spatial memory impairment and hippocampal neuroinflammation via inhibiting NF-κB activation in a rat model of Alzheimer's disease induced by amyloid-β(1-42).

Background: The neuroinflammation characterized by glial activation and release of proinflammatory mediators is considered to play a critical role in the pathogenesis of Alzheimer's disease (AD). Tetrandrine, a bisbenzylisoquinoline alkaloid isolated from the Chinese herb radix Stephania tetrandra, has been demonstrated to decrease the expression of proinflammatory mediators by inhibition of nuclear factor-κB (NF-κB) activation. The purpose of the study was to investigate effects of tetrandrine on experimental model of AD.