Cement Dust Exposure Alters Secretory Functions, Biochemical Profile and Morphology of Gastrointestinal Tissues in Rats Exposed to Cement Dust.

Asides direct gastrointestinal exposure, inhalation route is another major xenobiotic exposure pathway to the gastrointestinal tract via mucociliary escalator. This triphasic study assesses cement dust inhalatory exposure effect on the possible alterations of the gastrointestinal tissues and secretion. 72 male, sixteen (16) weeks old Wistar rats were randomized into 3 different phases of 24 animals. Each phase comprised of 3 group of 8 animals. Group 1 (control) were sham-operated with clean ambient air, group 2 (14-days exposed) were exposed to cement dust for 14days, and group 3 (28-day exposed) were exposed to cement dust for 28 days. Biochemical indices including superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), sulfhydryl group, carbonyl group, Na+-K+ATPase pump activity, Nitric oxide (NO) were investigated spectrophotometrically in gastric and hepatic tissues while histopathology was studied using standard procedure. There was significant increase in the level of MDA, NO and carbonyl- an observation that contrasts with the level of CAT, SOD and sulfhydryl; no significant difference in Na+-K+-ATPase pump was observed in the exposed groups compared with control. Histopathological alterations in salivary gland and gastric tissues includes edema, inflammatory cell infiltration and vascular congestion. There was significant alteration in basal salivary, gastric and biliary secretions; increased stimulated salivary and gastric secretion via cholinergic stimulation. Conclusively, histopathological and spectrophotometric analyses reflect that inhalatory experimental exposure to cement dust significantly alter gastrointestinal secretions and predisposes the gastrointestinal tract to an array of deleterious effects via protein oxidation and antioxidant depletion and tissue peroxidation.

Kolaviron attenuates ischemia/reperfusion injury in the stomach of rats.

Kolaviron (KV), an active complex of at least 3 compounds in Garcinia kola seed, which is known for its antioxidant and anti-inflammatory activity, was investigated for its gastro-protective effect in the stomach of rats subjected to ischemia/reperfusion-induced gastric ulceration. Male adult Wistar rats (180-210 g) were randomized into 6 groups (n = 15) as follows: (i) control, (ii) ulcerated untreated (UU), (iii) KV alone (KVA), (iv) KV + ulcer (KVU), (v) ulcer + KV (UKV), and (vi) ulcer + omeprazole (20 mg/kg). Ulcer was induced through ischemia/reperfusion method after 2 weeks of daily oral KV (100 mg/kg). Rats were weighed daily, and gastric acid secretion, ulcer scores, hematological, biochemical, and histological variables were assessed 1 h after induction at 3 and 7 days post-ulceration. Body weight decreased in KVA (179.1 ± 1.6 g), and KVU (170.1 ± 2.2 g) compared with UU (199.0 ± 1.4 g). Gastric acid secretion decreased significantly in KVU after 1 h and 3 days post-ulceration (0.27 ± 0.03 mEq/L; 0.49 ± 0.02 mEq/L) compared with UU (0.60 ± 0.06 mEq/L; 0.85 ± 0.29 mEq/L), respectively. There was significant reduction in neutrophil/lymphocyte ratio of KVA (0.29 ± 0.06) and KVU (0.35 ± 0.02) compared with UU (0.54 ± 0.04). Malondialdehyde level decreased significantly with concomitant increase in anti-oxidative activities and nitric oxide level in the KV treated groups (KVA, KVU, UKV) compared with UU. In conclusion, treatment with KV protects the stomach by reducing gastric acid secretion, promoting antioxidant activity and suppressing action of reactive oxygen species.

Seeds of Buchholzia coriacea in Diet Mitigate Ischemic Reperfusion-Induced Gastric Ulceration in Experimental Rats.

Buchholzia coriacea (B. coriacea) seeds, in folk medicine, have been documented to prevent gastric ulceration though the mechanism is not fully elucidated. To clarify this, the gastro-healing activities were investigated using graded incorporation of B. coriacea seeds in the diet. Male Wistar rats (150-200 g) were divided into 7 groups (n = 15): unulcerated untreated control, ulcerated untreated control, unulcerated B. coriacea low (10%), ulcerated B. coriacea low (10%), nulcerated B. coriacea high (25%), ulcerated B. coriacea high (25%), and ulcerated omeprazole-treated groups. Rats were fed with B. coriacea diets for 7 weeks; thereafter, ulcer was induced by ischemic reperfusion method. Daily body weight, gastric acid secretion, hematological parameters, stomach ulcer score, and biochemical and histological analyses were evaluated on days 0, 3, and 7 post-ulcer induction. Results were subjected to one-way analysis of variance (ANOVA) and presented as mean ± standard error of the mean (SEM); p ≤.05 was considered significant. Significant decreases were observed in mean body weight of B. coriacea-fed compared with control and omeprazole-treated groups from week 7. Ulcerated B. coriacea-fed showed significant decrease in gastric acid secretion by days 3 and 7 compared with ulcerated control groups. Malondialdehyde content was significantly decreased in ulcerated B. coriacea-fed compared with control and omeprazole-treated groups. Significant increases in hematological variables (notably platelet count), superoxide dismutase, catalase, and nitric oxide levels of B. coriacea-fed compared with control and omeprazole-treated groups by days 0 and 3 were observed. Histological evaluations further confirmed these observations. B. coriacea diet enhanced gastric healing activities on ischemic reperfused gastric ulcer. Increased platelet count and nitric oxide levels may play significant roles in this process.