Objective: To assess the effect of leaf extract of Persicaria lanigera on cotton pellet-induced granuloma tissue formation and acetic acid-induced ulcerative colitis. Methods: Rats were randomly divided into six groups: normal control, negative control, positive control (dexamethasone or sulfasalazine) as well as Persicaria lanigera (100-600 mg/kg)-treated groups. The effects of the extracts on body weight, antioxidant, and hematological parameters, as well as mast cell proliferation, were assessed. In addition, a histological evaluation was conducted. Results: Persicaria lanigera extract significantly decreased the mean exudate amount and suppressed granuloma tissue formation in a concentration-dependent manner in rats (P<0.05). Additionally, the extract significantly increased body weight, improved hematological profile, reduced the disease activity index score and malondialdehyde level, as well as enhanced catalase and superoxide dismutase activities (P<0.05). Histological evaluation showed Persicaria lanigera extract alleviated acetic acid-induced colonic damages, as evidenced by decreased cell necrosis, edema, and inflammatory cell infiltration. Conclusions: Persicaria lanigera extract possesses antiproliferative, antioxidative, and anti-colitis activities. However, its underlying mechanisms of action need further investigation.

Objective: To investigate the neuroprotective effect of C-phycocyanin in a mouse model of rotenone-induced Parkinson’s disease. Methods: C-phycocyanin (50 mg/kg, i.p., daily) was administered to rotenone (30 mg/kg, p.o., daily) treated mice for 28 days. Behavioral studies (Y-maze, rotarod, round beam walk, and wire-hang tests) were carried out to assess neurobehavioral deficits. Glutathione and malondialdehyde were determined in both serum and striatal tissue. Molecular proteins (AKT, AMPK, NF-κB, BDNF, and alpha-synuclein) in the striatum were estimated using ELISA. Histopathological analyses (hematoxylin and eosin stainning as well as Nissl staining) were carried out to assess structural abnormalities in the striatum. Results: C-phycocyanin significantly increased BDNF levels and decreased alpha-synuclein levels. It also slightly upregulated AMPK and AKT levels without significant difference compared with the rotenone group. Additionally, rotenone-induced elevated oxidative stress and structural abnormalities in the striatum were markedly mitigated by C-phycocyanin. Conclusions: C-phycocyanin might have potential neuroprotective effects against Parkinson’s disease. Further studies are warranted to verify its efficacy and to understand the molecular mechanisms behind the neuroprotective effects of C-phycocyanin in Parkinson’s disease.

Objective: To examine the hepatoprotective effects of gedunin in streptozotocin (STZ)-induced diabetic rats. Methods: Rats were divided into 4 groups: control, STZ, gedunin, and STZ+gedunin. Biochemical parameters for liver function and liver histology were studied. The molecular interaction of gedunin with the liver glucose transporters GLUT2 and SGLT1 was examined using AutoDock Vina. Results: Gedunin attenuated STZ-induced increase in the levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and gamma-glutamyl transferase in the serum and liver tissue, reduced lipid peroxidation, and enhanced antioxidant activity. Histopathological studies showed considerable restoration of liver architecture in gedunin-treated diabetic rats. In silico studies revealed stable binding of gedunin with GLUT2 and SGLT1. Conclusions: Gedunin exerts hepatoprotective effects in STZ-induced diabetic rats by reducing liver enzymatic activities and oxidative stress. Further studies are warranted to verify the mechanism of its hepatoprotective action.

Objective: To explore the effect of black radish (Raphanus sativus L. var niger) root extract on liver enzymes, oxidative stress, and histopathological alterations in mice with sodium valproate-induced hepatotoxicity. Methods: Thirty-two mice were divided into four groups: the control group received drinking water by gavage, the second group was administered with 100 mg/kg of sodium valproate, the third group received 300 mg/kg of black radish root extract, and the fourth group was given both sodium valproate (100 mg/kg) and black radish root extract (300 mg/kg). After 28 days, the mice were euthanized, and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), along with liver malondialdehyde (MDA), reactive oxygen species (ROS), mitochondrial parameters, tumor necrosis factor-alpha (TNF-α) gene expression, and histopathological changes were assessed. Results: Sodium valproate caused hepatic damage in mice, characterized by elevated serum levels of liver enzymes, increased MDA and ROS levels and TNF-α gene expression, as well as histopathological alterations. The black radish root extract significantly alleviated sodium valproate-caused hepatic injury by decreasing the serum levels of ALT and AST, MDA, ROS, TNF-α gene expression, as well as mitochondrial impairment, but did not have a significant effect on sodium valproate-induced histopathological changes. Conclusions: The black radish root extract demonstrates protective effects against sodium valproate-induced liver injury, possibly through mitigating oxidative stress, mitochondrial impairment, and inflammatory mediator expression.

Objective: To investigate the role of RPRD1B in the progression of diffuse large B-cell lymphoma (DLBCL) and its potential as a therapeutic target. Methods: This study analyzed RPRD1B expression in DLBCL and normal tissues using public databases and assessed its prognostic impact through survival analysis. In vitro and in vivo experiments were conducted to explore the mechanisms by which RPRD1B influences tumor growth and apoptosis. Results: RPRD1B expression was significantly elevated in DLBCL compared to normal tissues and was associated with poor prognosis. In vitro and in vivo experiments demonstrated that RPRD1B promoted lymphoma cell proliferation and inhibited apoptosis through the NF-κB signaling pathway. Conclusions: RPRD1B plays a critical role in the progression of DLBCL by modulating apoptosis and cellular proliferation. Targeting RPRD1B may offer a novel therapeutic strategy for DLBCL, suggesting its potential as a prognostic marker and therapeutic target in hematological malignancies.

In the article entitled “Boeravinone B ameliorates allergic nasal inflammation by modulating the GATA-3/T-bet signaling pathway in a mouse model of allergic rhinitis”, published on pages 245-252, Issue 6, Volume 14 in Asian Pacific Journal of Tropical Biomedicine, the weight number was misspelled as “18.5 g” on page 246, first line, under 2.2. Animals paragraph. The correct weight should be “(18.5±5) g”.