neda sistani karampour

 The therapeutic effects of bee pollen have already been proven in various studies, but toxicity studies in this field are limited. Therefore, in this study, the possible toxicity effects of hydroalcoholic extract of flower pollen on liver, kidney, and pancreatic tissues of male rats are investigated.

 Fourteen male rats were divided into two groups of seven: the first group received 800 mg/kg hydroalcoholic extract of bee pollen, and the second group received 0.5 mL/100 g normal saline intraperitoneally for 1 day. Then, their livers, kidney, pancreas, and oxidative stress biomarkers were evaluated. In addition, pieces of liver, kidney, and pancreatic tissues were examined histopathologically.

 Blood urea nitrogen (BUN) (P =0.0212), aspartate aminotransferase (AST) enzymes (P =0.0344), and malondialdehyde (MDA) biomarker (P =0.018) of kidney tissue were significantly decreased in the hydroalcoholic extract of bee pollen group compared to the control group. The glutathione (GSH) biomarker of kidney tissue showed a significant increase in this group compared to the control group (P =0.0031). The other evaluated parameters were not significantly different between the two groups (P> 0.05). Histopathologically, no deleterious and toxicity effects were observed in the tissues.

 Bee pollen has therapeutic properties and, as a nutrient, can be useful and effective for humans. In this study, this substance did not have toxicity effects on the liver, kidney, and pancreas and even protected vital organs in oxidative stress conditions. However, more research is needed to prove the toxicity of this valuable substance and to ensure its safety.

Parkinson’s disease (PD) is a common neurodegenerative disease characterized by progressive loss of midbrain dopaminergic neurons with multifactorial etiologies including age, genetic and environmental factors. The current treatments of the disorder only help reduce symptoms but not stop the disease progression. Morin has been shown to exert neuroprotective and anti-oxidant effects in different models of neurodegenerative diseases. This study aims to investigate the effects of morin on pseudo-parkinsonism induced by perphenazine in rats.

In an experimental study 40 male rats (weight range: 160-200 g) were randomly divided into 5 equal groups (n= 8). In group 1 (Reutononcy 3 mg/kg 48h and in 19 days) group 2 LDOPA (10mg/kg 48h 19days) group 3 (Reutcnonc 3mg/kg 48 h cinamicacid 50mg/kg 48h) group 4 (Reutcnonc 3mg/kg 48h and cinaminacid 100mg/kg 48h) group 5 (Reutcnonc 3mg/kg 48h and cinaminacid 200mg/kg 48h) in 19 days.In all groups The muscle stiffness, using Morpurgo method, rate of catalepsy using Rcaring test, and the amount of Malondialdehyde were avaluoted.

The results of study reported the effectiveness of cinamicacid on improving muscle stiffness and muscle weakness, which it was dose dependent, so that cinamicacid at higher doses was more effective in improving these two complications. Moreover, the results reported the effect of different doses of cinamicacid on the reduction of MDA.

 Idiopathic pulmonary fibrosis (IPF) is a progressive fatal disease affecting the lung, and currently there is no efficient therapy for this condition. Curcumin, as a natural anti-inflammatory and antioxidant agent, could repress the pulmonary fibrosis (PF) caused by Bleomycin (BLM).

 The aim of the research was to evaluate the protective activity of a nano-formulation of curcumin administered by inhalation on BLM-induced PF in rats.

 Eighty rats were randomly divided into eight experimental groups. Group one (control) that received saline intratracheally (IT) and subjected to vehicle inhalation. Group two to eight each received a single dose of BLM (5 IU/kg, IT) along with vehicle inhalation, oral prednisolone, oral curcumin, curcumin inhalation, and nano-curcumin inhalation with the doses of 50, 100, and 200 µg/kg, respectively. In the control and other groups, BLM was injected intratracheally on the first day of the experiment. In the treatment groups, curcumin suspension was prepared in distilled water and applied through nebulization for 21 consecutive days after BLM intratracheal administration. Then the rats were euthanized, and inflammatory cytokines (TNF-α, TGF-β, PDGF), hydroxyproline, and IL-10 (as a protective cytokine) were measured. Also, lung histopathological features were examined.

 The synthesized nano-formulation reduced the overall hydroxyproline content of lungs in BLM-treated rats (P < 0.002). In addition, TNF-α, TGF-β, and PDGF levels significantly increased in the lungs of BLM-instilled rats (P < 0.001). However, the nano-formulation of curcumin (200 µg/kg) significantly decreased the levels of these inflammatory cytokines (P < 0.001) and increased IL-10 level (P = 0.0144) compared with the control group.

 The nebulization of nano-curcumin is suggested as a novel approach for the treatment of PF induced by BLM in rats. Our findings revealed that the inhalation (as a safe local drug delivery system approach) of the nano-curcumin at a dose of 200 µg/kg (formulated by cyclodextrin) could effectively protect the lung against PF.

Idiopathic pulmonary fibrosis (IPF) is a fatal and incurable lung disease. Morin, a natural product with antioxidant and anti-inflammatory activity, could reduce lung inflammation induced by lipopolysaccharide (LPS) and liver fibrosis in previous studies.

The aim of this study was to evaluate the antifibrotic activity of morin in the pulmonary fibrosis induced by bleomycin in mice.

Pulmonary fibrosis was induced by the intratracheal instillation of bleomycin (3 mg/kg) in C57Bl/6J mice. Morin (10, 20, and 40mg/kg, p.o.) was given to mice from day 0 to 21 after bleomycin administration. The mice were sacrificed on day 21 to measure the total number of cells, the percentage of leukocytes in bronchoalveolar lavage fluid (BALF), lung hydroxyproline content, lung index, and oxidative stress markers. Histopathological changes were evaluated by the microscopic examination of sections stained with hematoxylin-eosin and Masson’s trichrome.

Our data showed that treatment withmorin significantly attenuated the infiltration of inflammatory cells, hydroxyproline content, lung index, and oxidative stress that were elevated in fibrotic lungs. In addition, morin could reduce the pathological changes induced by bleomycin.

Based on the study, morin, probably by its anti-inflammatory and antioxidant activities, can attenuate pulmonary fibrosis induced by bleomycin in mice.