Sinapic acid (SA) is a natural pharmacological active compound found in berries, nuts, and cereals. The current study aimed to investigate the protective effects of SA against thioacetamide (TAA) fibrosis in rats by histopathological and immunohistochemical assays. The albino rats (30) were randomly divided into five groups (G). G1 was injected with distilled water 3 times/week and fed orally daily with 10% Tween 20 for two months. G2–5 were injected with 200 mg/kg TAA three times weekly for two months and fed with 10% Tween 20, 50 mg/kg silymarin, 20, and 40 mg/kg of SA daily for 2 months, respectively. The results showed that rats treated with SA had fewer hepatocyte injuries with lower liver index (serum bilirubin, total protein, albumin, and liver enzymes (ALP, ALT, and AST) and were similar to that of control and silymarin-treated rats. Acute toxicity for 2 and 4 g/kg SA showed to be safe without any toxic signs in treated rats. Macroscopic examination showed that hepatotoxic liver had an irregular, rough surface with micro and macro nodules and histopathology expressed by Hematoxylin and Eosin, and Masson Trichrome revealed severe inflammation and infiltration of focal necrosis, fibrosis, lymphocytes, and proliferation bile duct. In contrast, rats fed with SA had significantly lower TAA toxicity in gross and histology and liver tissues as presented by less liver tissue disruption, lesser fibrosis, and minimum in filtered hepatocytes. Immunohistochemistry of rats receiving SA showed significant up-regulation of HSP 70% and down-regulation of alpha-smooth muscle actin (α-SMA) protein expression compared to positive control rats. The homogenized liver tissues showed a notable rise in the antioxidant enzymes (SOD and CAT) actions with significantly lower malondialdehyde (MDA) levels compared to that of the positive control group. Furthermore, the SA-treated rats had significantly lower TNF-a, IL-6, and higher IL-10 levels than the positive control rats. Thus, the findings suggest SA as a hepatoprotective compound due to its inhibitory effects on fibrosis, hepatotoxicity, liver cell proliferation, up-regulation of HSP 70, and downregulation of α-SMA expression, inhibiting lipid peroxidation (MDA), while retaining the liver index and antioxidant enzymes to normal.

Pinostrobin (5-hydroxy-7-methoxyflavanone; PN) is a natural active ingredient with numerous biological activities extensively utilized in tumour chemotherapy. The present study investigates the chemo-preventive potentials of PN on azoxymethane-mediated colonic aberrant crypt foci in rats. Sprague Dawley rats clustered into five groups, normal control (A) and cancer controls were subcutaneously injected with normal saline and 15 mg/kg azoxymethane, respectively, and nourished on 10% tween 20 and fed on 10% tween 20; reference control (C), injected with 15 mg/kg azoxymethane and injected (intraperitoneal) with 35 mg/kg 5-fluorouracil (5-FU); D and E rat groups received a subcutaneous injection of 15 mg/kg azoxymethane and nourished on 30 and 60 mg/kg of PN, respectively. The acute toxicity trial showed a lack of any abnormal signs or mortality in rats ingested with 250 and 500 mg/kg of PN. The gross morphology of colon tissues revealed significantly lower total colonic aberrant crypt foci incidence in PN-treated rats than that of cancer controls. Histological examination of colon tissues showed increased aberrant crypt foci availability with bizarrely elongated nuclei, stratified cells and higher depletion of the submucosal glands in cancer controls. PN treatment caused positive modulation of apoptotic (Bax and Bcl-2) proteins and inflammatory cytokines (TNF-α, IL-6 and IL-10). Moreover, rats fed on PN had significantly higher antioxidants (superoxide dismutase) and lower malondialdehyde concentrations in their colon tissue homogenates. The chemoprotective efficiency of PN against azoxymethane-induced aberrant crypt foci is shown by lower aberrant crypt foci values and higher aberrant crypt foci inhibition percentage, possibly through augmentation of genes responsible for apoptotic cascade and inflammations originating from azoxymethane oxidative stress insults.

The liver has a tremendous regeneration potential, yet chronic liver injury poses a life-threatening condition if not managed appropriately. Apocynin, an N

Helicobacteriosis is a common bacterial infection caused by Helicobacter pylori. It affects the stomach and small intestines, leading to inflammation. Bacteria can spread through contaminated food or water. This review explores the role of food in the transmission of H. pylori, drawing on research from the past three decades. People commonly acquire the infection during childhood, often from close family members. Crowded living conditions can also contribute to the spread. This review also discusses various risk factors and highlights the challenges of detecting H. pylori, particularly in its dormant form. Techniques like ribotyping and restriction fragment length polymorphism hold promise for tracing transmission routes, but more long-term studies are needed to account for potential confounding factors.

Toxoplasmosis is a significant food-borne zoonotic disease that causes a wide range of clinical syndromes in humans, including pregnant women, immunosuppressed individuals, land and sea mammals, and various bird species. Felidae is the only definitive host that excretes a million oocysts of T. gondii in their feces, polluting the environment. T. gondii has a complex life cycle, with sexual reproduction occurring in cats, where oocysts are formed and excreted with feces. The meiosis of oocysts in the environment leads to the formation of sporozoites that are infectious to intermediate hosts, such as rodents and livestock animals. In these intermediate hosts, rapidly replicating tachyzoites are disseminated throughout the body, forming tissue cysts containing bradyzoites. Infected individuals become infected by ingesting oocysts from contaminated soil, water, or food. The transmission of toxoplasmosis is recognized as zoonotic transmission, with the primary route being through the ingestion of contaminated food or water, particularly undercooked or raw meat, and unwashed fruits and vegetables that have come into contact with the parasite’s oocysts. The signs and symptoms of toxoplasmosis can vary widely, with most healthy individuals having a normal immune system and mild symptoms resolving on their own.