Peptic ulcer disease is the greatest digestive disorder that has increased incidence and recurrence rates across all nations. Prangos pabularia (L.) has been well documented as a folkloric medicinal herb utilized for multiple disease conditions including gastric ulcers. Hence, the target study was investigation the gastro-protection effects of root extracts of Prangos pabularia (REPP) on ethanol-mediated stomach injury in rats. Sprague Dawley rats were clustered in 5 cages: A and B, normal and ulcer control rats pre-ingested with 1 % carboxymethyl cellulose (CMC)); C, reference rats had 20 mg/kg omeprazole; D and E, rats pre-supplemented with 250 and 500 mg/kg of REPP, respectively. After one hour, group A was given orally 1 % CMC, and groups B-E were given 100 % ethanol. The ulcer area, gastric acidity, and gastric wall mucus of all stomachs were determined. The gastric tissue homogenates were examined for antioxidant and MDA contents. Moreover, the gastric tissues were analyzed by histopathological and immunohistochemically assays. Acute toxicity results showed lack of any toxic effects or histological changes in rats exposed to 2 and 5 g/kg of REPP ingestion. The ulcer controls had extensive gastric mucosal damage with lower gastric juice and a reduced gastric pH. REPP treatment caused a significant reduction of the ethanol-induced gastric lacerations represented by an upsurge in gastric mucus and gastric wall glycoproteins (increased PAS), a decrease in the gastric acidity, leukocyte infiltration, positively modulated Bax and HSP 70 proteins, consequently lowered ulcer areas. REPP supplementation positively modulated oxidative stress (increased SOD, CAT, PGE2, and reduced MDA) and inflammatory cytokines (decreased serum TNF-α, IL-6, and increased IL-10) levels. The outcomes could be scientific evidence to back-up the folkloric use of A. Judaica as a medicinal remedy for oxidative stress-related disorders (gastric ulcer).

The prevalence of gastric ulcers has increased in recent years, mainly because of non-steroidal anti-inflammatory drug utilization. Therefore, the current study investigates the gastroprotective effect of p-Cymene on absolute ethanol-induced acute gastric mucosal hemorrhagic lesions in rats. Thirty Sprague Dawley rats were randomly separated into five groups: normal control, ulcer control, reference, and two experimental groups. The normal and ulcer control groups were orally fed with 0.5% carboxymethylcellulose (CMC). The reference group was fed orally with 20 mg/kg omeprazole. The experimental groups were fed with 30 mg/kg and 60 mg/kg p-Cymene, respectively. After one hour, the normal group was fed with 0.5% CMC, and groups 2–5 were given absolute alcohol. After another hour all rats were sacrificed. The ulcer control group showed severe superficial hemorrhagic gastric mucosal lesions with decreased gastric mucus secretion and pH of gastric content. p-Cymene significantly reduced ethanol-induced gastric lesions, as evidenced by increased mucus and pH of gastric content, decreased ulcer area, reduced or absence of edema, and leucocyte infiltration of the subcutaneous layer. In gastric mucosal homogenate, p-Cymene displayed a significant increase in superoxide dismutase (SOD), catalase (CAT) activities, prostaglandin E2 (PGE2), and significantly reduced the malondialdehyde (MDA) level. In addition, p-Cymene increased the intensity of periodic acid–Schiff (PAS) stain of the gastric epithelium, and produced up-regulation of the HSP 70 protein and down-regulation of the Bax protein of the stomach epithelium, as well as a reduction in the levels of tumor necrotic factor-alpha and interleukin-6, while the level of interleukin-10 was increased. p-Cymene decreased the level of TNF-a and IL-6, and increased the level of IL-10. Acute toxicity with a higher dose of 500 mg/kg p-Cymene did not manifest any toxicological signs in rats and could enhance defensive mechanisms against gastric mucosal lesions. p-Cymene showed gastroprotective effects that could be attributed to its antioxidant nature, or its ability to increase mucus secretion, increase endogenous enzymes (SOD, CAT, PGE2), reduce MDA level, up-regulate HSP 70 protein, down-regulate Bax protein, and modulate inflammatory cytokines.

The study in vivo assessed the effect of pinostrobin on the histology, immunohistochemistry, and biochemical parameters of thioacetamide (TAA) induced liver cirrhosis in Sprague Dawley rats. The rats were noticeably gavaged with two doses of pinostrobin (30 mg/kg and 60 mg/kg) with TAA and exhibited a substantial decrease in the liver index and hepatocyte propagation with much minor cell injury. These groups meaningfully down-regulated the proliferation of cellular nucleus antigen (PCNA) and alpha-smooth muscle actin (α-SMA). The liver homogenate displayed augmented antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activities escorted with reducing in malondialdehyde (MDA) level. The serum level of bilirubin, total protein, albumin, and liver enzymes (ALP, ALT, and AST) returned to normal and was similar to that of normal control and silymarin with TAA-treated groups. pinostrobin-fed groups also decreased the level of Tumor necrosis factor-alpha (TNF-α), Interleukin-6 (IL-6), and increased the level of Interleukin-10 (IL-10). Acute toxicity with a higher dose of 500 mg/kg of pinostrobin did not manifest any toxicological signs in rats. The hepatoprotective effect of pinostrobin could be due to potentially inhibited the progression of liver cirrhosis, down-regulation of PCNA and α-SMA proliferation, prevented oxidation of hepatocytes, improved SOD and CAT enzymes, condensed MDA, repairs of liver biomarkers, reduced cellular inflammation and modulation of inflammatory cytokines.

This research in vivo assessed the impact of the ethanolic extract of Annona muricata (A. muricata) on the histopathology, immunohistochemistry, and biochemistry of thioacetamide (TAA)-induced liver cirrhosis in Sprague Dawley rats. The rats, gavaged precisely with two doses of A. muricata (250 mg/kg and 500 mg/kg) with TAA, presented a substantial reduction in the liver index and hepatocyte propagation, with much lower cell injury. These groups showed meaningfully down-regulated proliferating cell nuclear antigen (PCNA) in the liver and spleen, α-smooth muscle actin (α-SMA), and transforming growth factor-beta 1 (TGF-β1) in liver parenchymal tissue. The liver homogenate displayed enhanced antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activity, along with a decrease in malondialdehyde (MDA) levels. The serum levels of bilirubin, total protein, albumin, and liver enzymes alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were returned to normal and were similar to that of the normal control and silymarin with TAA-treated groups. Oral acute toxicity revealed no evidence of any toxic symbols or mortality in rats, indicating the safety of A. muricata. Therefore, the normal microanatomy of hepatocytes, the clampdown of PCNA, α-SMA, TGF-β, improved antioxidant enzymes (SOD and CAT), and condensed MDA with repairs of liver biomarkers validate the hepatoprotective effect of A. muricata.

Gynura procumbens is an edible flowering plant that has been utilized as traditional therapy for numerous diseases. The current experiment investigates the hepatoprotective potentials of the ethanol extract of Gynura procumbens leaf (EEGPL) against thioacetamide (TAA)-induced liver cirrhosis in rats. Thirty Sprague Dawley rats were randomly divided into 5 clusters: A, rats received orally 10% Tween 80 and intraperitoneal (i.p) inoculation of sterile distal water; B, rats received orally10% Tween 80; C, rats received orally daily 50 mg/kg of silymarin, while groups; D and E, rats received orally daily doses of 200 and 400 mg/kg of EEGPL, respectively. Furthermore, B-E clusters received 200 mg/kg thioacetamide (i.p) three times a week for 60 days.

The protective effect of biochanin A (BCA) on the histopathology, immunohistochemistry, and biochemistry of thioacetamide (TAA)-induced liver cirrhosis in vivo was investigated. There was a significant reduction in liver weight and hepatocyte propagation, with much lower cell injury in rat groups treated with BCA (25 mg/kg and 50 mg/kg) following a TAA induction. These groups had significantly lower levels of proliferating cell nuclear antigen (PCNA) and α-smooth muscle actin (α-SMA). The liver homogenates showed increased antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as decreased malondialdehyde (MDA) levels. The serum biomarkers associated with liver function, namely alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyl transaminase (GGT), returned to normal levels, comparable to those observed in both the normal control group and the reference control group. Taken together, the normal microanatomy of hepatocytes, the inhibition of PCNA and α-SMA, improved antioxidant enzymes (SOD, CAT, and GPx), and condensed MDA with repairs of liver biomarkers validated BCA’s hepatoprotective effect.